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 http://www.archive.org/details/cu31924000310940 
 
[ 993 ] 
 N ' lOoio 
 
 XXIIT. The Croonian Lectuee. — On the Rhythm of the Heart of the Frog, and 
 on the Nature of the Action of the Vagus Nerve. 
 
 Bij W. H. Gaskell, M.D., Cant. 
 
 Communicated by Br. Michael Foster, Sec. R.S.,fi'om the Physiological Laboratory, 
 
 Carnhridge. 
 
 Received December 8,— Read December 22, 1881. 
 
 [Plates 66-70.] 
 
 In all investigations upon the causation of the beat of the heart, one question stands 
 forwai'd prominently before all others, viz. : What is the relative share taken by the 
 ganglion cells and the muscular tissue respectively in the production of its spontaneous 
 rhythmical beats ? And in any discussion upon the action of the cardiac nerves, the most 
 important question always is. How far do they act on the ganglion cells, how far on 
 the muscular tissue directly? 
 
 In recent times a variety of investigations have pointed unmistakably to the con- 
 clusion that rhythmical action can occur in muscular tissue under the influence of a 
 constant stimulus without the intervention of ganglion cells, or at all events of any 
 well-defined recognisable nerve-cells ; in other words, certain kinds of muscular tissue 
 possess the faculty of transforming the effects of a continuous stimulus into a dis- 
 continuous result. 
 
 Again, there can be no doubt whatever that in the heart of the Frog the rhythmical 
 beat is markedly associated with the presence of certain ganglion cells, especially the 
 cells of Remak's ganglia, so that the first question which it is absolutely necessary to 
 answer is, Does the normal rhythm of the heart as a whole depend upon separate 
 rhythmical impulses passing from certain motor ganglia to the muscular tissue, each of 
 which impulses causes a contraction, so that the rhythm is due to the nerve cells, and 
 the muscle simply gives expression to it, or do the motor cells send to the muscles a 
 continuous series of subminimal impulses, the effects of which the muscle sums up, so 
 as to produce from time to time a single beat ; in other words, Is the rhythm due to 
 the muscle, while the nerve cells supply the constant stimulus ? 
 
 Further, before it is possible to consider the action of the cardiac nerves, it is neces- 
 sary to come to some conclusion respecting the different attributes of the cardiac 
 muscle apart from the question of rhythm, and it seems to me that the three which 
 especially demand attention are the following : — 
 
 6 L 2 
 
 V/./ 
 
994 DR. W. H. GASKELL OX THE RHYTHM OF THE HEART OF 
 
 1. Contraction-power, as measured by the extent of the contraction. 
 
 2. Excitabihty, as measured by the response or non-response of the muscle to the 
 
 stimulus. 
 
 3. Tonicity, as measured by the extent of the relaxation of the tissue at the 
 
 commencement of each contraction. 
 
 I propose, then, to discuss in the first part of this paper not only the nature of the 
 normal rhythm of the heart, but also certain variations in the three above-mentioned 
 attributes of the cardiac muscle, together with their relations to each other. After- 
 wards I will proceed to the second part and endeavour to determine the respective 
 actions of the vagus nerve upon the ganglion cells and the cardiac muscle. 
 
 In order to investigate the different problems suggested above, it is clearly necessary 
 to employ the graphic method, and at the same time it is very advisable to obtain a 
 method which shall register simultaneously as many of the different factors involved 
 
 as possible. 
 
 As far as the question of tonicity is concerned, I have chiefly made use of the 
 arrangement described in my paper'" " On the Tonicity of the Heart and Blood-vessels," 
 and those experiments I propose to consider later on ; there are, however, considerable 
 difficulties of interpretation in using this method for the determination of the force of 
 contraction of different parts of tlie heart. I therefore resolved to investigate the 
 nature of the cardiac contractions in the bloodless heart after the same plan as has 
 been used with such marked success in the case of ordinary striped muscle and its 
 nerve. 
 
 The vagus nerve, usually on the left side, is dissected out so as to be as long as possible, and a ligature 
 attached to one end ; the two aortic trunks are cut close to the bulbus, and a thread is tied to the 
 extremity of the loose auricular flap, at the junction of the two auricles, which is exposed by the removal 
 of the aortic trunks ; another thread is attached to the extreme apex of the ventricle, and the heart with 
 a piece of the oesophagus and trachea behind it, and with the vagus nerve intact, is removed from the 
 body. In taking the heart out the lungs are cut away, and the venous sinus carefully left intact. One 
 of Keoneckee's forceps is now made to clip the free end of the oesophagus and trachea, and held tight in 
 a suitable holder (Plate 66, F). The thread attached to the auricles is fixed by means' of a small hook to 
 a lever A which is capable of movement in a vertical plane, while that attached to the ventricle is fixed 
 in a similar way to another exactly similar lever B, which can slide up and down on the same support 
 below the lever A. The upper lever to which the auricles are attached is drawn up above the horizontal 
 position by means of an elastic thread fixed to it near the fulcrum, and also fixed to the support above it, 
 as is seen at C in the figure. In this way the heart is suspended between the two levers A and B, the 
 lower one of which is drawn upwards by its contraction, the upper one downwards. Between the two a 
 clamp D is now placed so as just to hold the tissue tight in the auriculo-ventricular groove, and the two 
 levers are adjusted so that they are parallel and horizontal. The clamp is made of two limbs of strong 
 but thin metal with carefully rounded edges, which are capable of being approximated to each other by 
 means of a fine micrometer screw. The levers are provided with aluminium-foil points, and are adjusted 
 so that the two wi'iting-points are exactly in the same vertical line when the levers are horizontal. By 
 
 * Journal of Physiol., vol. iii., p. 48, 
 
THE FROG, AND ON THE ACTION OF THE VAGUS NERVE. 995 
 
 means of a drum the two levers write at tlie same moment upon tlie blackened paper, and tlie upper 
 lever moving downwards records the contractions of the auricle, while the lower lever moving upwards 
 traces those of the ventricle. 
 
 The vagus nerve is now laid upon a pair of platinum electrodes B, and kept moist by laying over it a 
 piece of filter paper dipped into normal saline solution. The electrodes are in connexion with an ordinary 
 induction coil driven by a single Daniell cell, the interrupter of which is a tuning-fork instead of the 
 usual hammer. In addition to the two tracings described above, the usual time and stimulation markers 
 write on the blackened paper. 
 
 In the description just given 1 have spoken of the clamp as being placed in the 
 anriculo-ventricular groove, so as to register the auricular and ventricular contractions 
 simultaneously ; it can, however, be placed across any portion of the heart, for example 
 between the sinus and auricles, so as to register the sinus and auricular contractions ; 
 midway between the base and the apex of the ventricle, so as to register the contrac- 
 tions of the base and apex simultaneously, &c. 
 
 Besides the advantage obtained by the power of registering at will the contractions 
 of any two contiguous parts of the heart, the clamp enables us to study the efiects of 
 compression at different points much more delicately than the old plan of ligaturing, for 
 it is possible either just to hold the tissue so as not to injure it physiologically or to com- 
 press it up to any required amount by the simple movement of the micrometer screw. 
 
 Further, it is possible to cut the ventricle open from base to apex, and to apply 
 poisons or fluids of any kind to that part of the heart which is situated below the 
 clamp without any chance of their reaching the parts above the clamp (the latter being 
 provided with a flange on each side to prevent the fluids passing over it). Also the 
 parts on the one side of the clamp can be heated or cooled independently of the parts 
 on the other side, and under all these different conditions the effect of stimulation of 
 the vagus nerve can be' studied. Throughout the course of each experiment the heart 
 is kept moist by the application of salt solution. 
 
 PART I. 
 On the Ehythm of the Heart. 
 
 If we imagine a portion of muscle made to contract rhythmically by the action of 
 certain cells situated at a distance from it, then it is clear that the rate of rhythm will 
 be independent of any increase in the excitability of the muscle, if the rhythm is due 
 to separate impulses passing from the cells to the muscles, each of which is able to 
 cause a contraction ; on the other hand, an increase in the muscular excitability must 
 cause a quicker rate of rhythm, if the rhythm is dependent upon some process of 
 summation of stimuli taking place in the muscle itself. 
 
 Now, by the method described above it is possible to influence in different ways 
 either the ventricle alone on the one side of the clamp without afi'ecting the sinus and 
 auricles on the other side, or only the auricles and other parts on that side of the 
 
990 DR. W. H, CtASKELL ON THE RHYTHM OP THE HEART OP 
 
 clamp without touching the ventricle ; so that it is possible to increase or diminish the 
 excitability of the ventricular muscle ^^ithout afi'ecting the discharges from the motor 
 ganglia, or to act upon the motor ganglia without altering the excitability of the 
 ventricle. Of the various means for effecting this object, it will be sufficient to give 
 examples of the action of heat, atropin and muscarin. 
 
 When the whole heart is heated the rate of rhythm is always greatly increased, 
 and the same, as is well known, is true in the case of eithe-r the ventricle or apex when 
 isolated and beating spontaneously. In this latter case the greater rapidity of rhythm 
 is partly, at all events, to be ascribed to the increase of excitability in the muscle due 
 to the heating. 
 
 Suppose, now, in the heart suspended as described above the ventricle alone be heated, 
 then its excitability will be increased* while that of the auricles will remain the same 
 as before, and therefore if the rhythm be dependent upon the muscular tissue, as in the 
 case of the isolated apex, the ventricle ought to beat at a quicker rate than the 
 auricles whose excitability has not been altered. On the other hand, if the rhythm is 
 due to discrete impulses passing from the motor gangha to the ventricle, then no 
 increase in the excitability of the latter ought to make the smallest alteration in the 
 rate of the beats, because upon that view the ventricle does not contract except when 
 an impulse reaches it, and the motor ganglia remaining outside the range of the heating 
 the rate at which their discharges take place remains unaltered and is unaffected by 
 any alteration in the excitability of the ventricular muscle. Of these two views 
 experiment proves that the latter is the true one. 
 
 If the clamp be placed in the auriculo-ventricular groove and be tightened so as 
 just to hold the tissue firmly, then both auricles and ventricle continue to beat with 
 perfect regularity for hours, each ventricular beat following in orderly sequence upon 
 each auricular. In order to heat the parts of the heart on one side of the clamp 
 without heating those on the other side I have used a spiral of thin platinum or 
 copper wire which is placed round either the ventricle or the auricles and sinus and 
 is in connexion by means of a key with a battery of two or three Grove cells. When 
 the ventricle alone is to be heated it is placed in connexion with the upper lever and 
 the auricles with the lower ; if the heating is intended to affect only the sinus and 
 auricles then the arrangement is reversed. That this method- works well is shown by 
 the fact that whereas a thermometer suspended within the spiral may show a rise up to 
 50° or 60° C. under the heating influence of three Grove cells, yet a thermometer 
 placed against the tissue just below the clamp does not show any rise at all, when the 
 spiral is in position round that part of the heart which is situated above the clamp. 
 
 Heating the sinus and auricles alone in this way causes a most marked increase in 
 
 the rate of rhythm both of the auricles and ventricle, with other phenomena which 
 
 will be mentioned presently (Plate 67; fig. 1), showing that the method of heating is 
 
 effective. On the other hand, when the ventricle alone is heated no alteration in the 
 
 * Keoneckbe, " Das cliaract. Merkmal der Herzrauskel-Beweg." Ludwig's Pestgabe, 1874. 
 
THE FROG, AND ON THE ACTION OE THE VAGHS NEiiVE. 997 
 
 rate of rhythm either of ventricle or auricles is jDroduced ; the rate of the auricular 
 beats continues the same ; the ventricular beat follovi'S upon each auricular with the 
 same regularity as before, and, in fact, as far as the rhythm is concerned the ventricle 
 might not have been heated (Plate 67, fig. 2). That the heating was effective, however, 
 the figure clearly shows, lor the force of the ventricular contractions is markedly 
 diminished during the time that the muscle was heated : a fact of considerable 
 importance, as proving that heat acts U})on the muscular tissue of the heart in such a 
 Avay as to diminish the force of its contractions apart altogether from the rapidity of 
 the rate of rhythm of those contractions. 
 
 This experiment seems to me positive proof that in the whole heart the rhythm is 
 due to discrete impulses proceeding from certain motor ganglia to the muscular tissue, 
 each of which impulses causes a contraction of that tissue. Further evidence to the 
 same efl:ect is given by a series of results which may be generalized as follows : — 
 
 Any influence which, applied to the auricles and sinus alone, causes an cdteration 
 in the rhythm of the auricles, affects the rate of the ventricular beats synchronously, 
 while the same influence, applied to the ventricle alone, causes no initial alteration in 
 the rhythm either of ventricle or auricles. 
 
 Thus cold slows both the auricular and ventricular beats when applied to the 
 auricles and sinus, while the same amount of cold produces no effect on the rhythm 
 when apphed to the ventricle alone. Atropin sulphate (1 p.c. solution) dropped on to 
 the auricles and sums slows the rate of beating of the whole heart most markedly 
 (Plate 70, fig. 26 B) while the same solution applied to the cut-open ventricle produces 
 no initial effect upon the rhythm. So, too, with muscarin sulphate, a marked slowing 
 when applied to the auricles and sinus ; no alteration of rhythm, for some time at all 
 events, when confined to the ventricle. (See Plate 70, figs. 26 A, 27.) 
 
 Many more instances of the same kind might be given, but enough has been said 
 already to permit us to formulate the following proposition : — ■ 
 
 The rhythmical contractions of the heart as a whole are caused by discrete impulses 
 lohich proceed rhythmically from certain motor ganglia to the auricles and ventricle. 
 
 The apparent discrepancy between this assertion and the rhythmical phenomena 
 exhibited by the isolated ventricle and apex will be discussed at the end of this part 
 of my subject. 
 
 On the want of sequence bettveen the ventricular and auricular contractions. 
 
 If, however, we conclude that separate impulses pass from the motor ganglia to the 
 ventricle, the further question arises, What conditions are necessary so that each one 
 of these impulses should cause a contraction of the ventricular muscle ? 
 
 In the ventricle or apex alone we know, from the experiments of Kronecker,"" that 
 
 * Op. cit. 
 
998 DR. W. H. GASKELL ON THE RHYTHM OP THE HEART OE 
 
 a series of single induction shocks of sufficient strength, sent through the muscle at a 
 definite and invariable rate, will cause a synchronous series of contractions ; and that 
 if then the muscle be cooled down, the same series of single stimuli will cause a series 
 of contractions synchronous not with every stimulus, but with every second stimulus. 
 Again, V. Basch'' has shown that a series of single stimuli of the same strength may 
 cause a series of contractions synchronous with every second stimulus when each 
 stimulus is so weak as to be unable to cause a contraction by itself. 
 
 From these two observations we may draw the conclusion that a definite relation 
 between the strength of the stimulus and the excitability of the ventricular muscle is 
 necessary, in order that the muscle should contract synchronously with the series of 
 artificial stimuli ; and also that the muscle may be made to respond synchronously to 
 every second stimulus, instead of to every stimulus, either by lowering the excitability 
 of the muscle, the strength of the stimulus remaining unaltered, or by lessening the 
 stimulus, while the excitability remains the same. 
 
 In his latest paper,t v. Basch suggests as an explanation of this half-rhythm that 
 a stimulus which is insufficient to cause a contraction increases the excitability of the 
 muscle, so that a subsequent stimulus of the same strength is thereby enabled to 
 produce a contraction. 
 
 These observations of Kroneckek and v. Basch may be taken as evidence that the 
 ventricular muscle is able to sum up the effects of two or even more artificial stimuli ; 
 but so far we have no proof that it is able to act in the same way towards the normal 
 impulses coming from the motor ganglia. 
 
 This evidence I have been able to supply by my method of experimentation, and 
 have come to the conclusion that a definite relation between the strength of the 
 impulses from the motor ganglia, and the excitability of the ventricular muscle, is 
 requisite to ensure the occurrence of a series of ventricular beats synchronous with the 
 impulses coming from the motor ganglia. Here, too, j ast as in the case of the artificial 
 stimuli, a certain number of the impulses prove inefficient to cause a contraction when 
 the excitability of the muscle is lowered sufficiently ; here, too, a diminution in the 
 strength of the impulses below a certain limit causes the ventricle to beat synchronously 
 with every two, three, or more impulses, instead of with every impulse, although the 
 excitability of the muscle remains the same. 
 
 In this case, then, as well as in the case of artificial stimulation, the probable 
 explanation of the half-rhythm observed is to be found in the following extension of 
 the suggestion made by v. Basch, viz. : ivhen the relation between the strength of the 
 im'pulses coming from the motor ganglia and the excitability of the ventricular muscle 
 is such that each separate impulse is not able to cause a beat of the ventricle then the 
 ventricle does not necessarily remain qiiiescent, but beats synchronously tvith every second 
 
 * Sitzber. d. k. Akacl. d. Wiss. (Wien.) Bd. Ixxix., III. Abtli. 
 t Arch. f. Anat. u. Physiol. (Physiol. Abth.). 1880, S. 283, 
 
THE FROG, AND ON THE ACTION OF THE VAGUS NERVE. 999 
 
 impulse, because each impulse, though unable to cause a contraction of the muscle, may 
 increase its excitability to the height necessary for the production of a beat by the time 
 the next impulse reaches the tissue. 
 
 The proof of these assertions depends upon the fact that^ by the method of clamping, 
 it is possible to alter the relation between the strength of the impulses and the 
 excitability of the ventricular muscle without affecting the relation between the motor 
 ganglia and the auricular muscle. The rate, therefore, at which the impulses are sent 
 out from the motor ganglia is indicated by the rate of the auricular beats, and the 
 extent of synchronism between them and the beats of the ventricle determines the 
 number of impulses that have been made inefficient, as far as the causation of a 
 ventricular beat is concerned, by the action of each special operation. 
 
 This want of sequence between the auricular and ventricular contractions can be 
 obtained by three different methods. 
 
 1. By tightening the clamp in the auriculo- ventricular groove. 
 
 2. By heating the auricles and sinus without heating the ventricle. 
 
 3. By the application of various poisons to the ventricle alone. 
 
 By the use of the micrometer screw attached to the clamp it is possible to compress 
 the tissue so slightly, and yet to hold it with sufficient firmness, that the sequence of 
 ventricular upon auricular beats continues without alteration or interruption ; it is 
 possible also to compress it so strongly that the motor impulses can no longer reach 
 the ventricle, and therefore the ventricle remains quiescent, while the auricles continue 
 beating with unaltered rhythm ; and it is possible to compress it to any extent inter- 
 mediate between these two extremes, and to observe the alteration in the ventricular 
 rhythm so produced. This latter case is that with which we are specially concerned at 
 present, and in every instance I have found that with gradual tightening of the clamp 
 the ventricle does not pass abruptly into a state of quiescence, but that the increased 
 compression always causes the ventricle to beat slower than the auricles. This slower 
 rate of beating is never independent of the auricular rate, but is connected with it in 
 such a way that the ventricle, instead of beating synchronously with each beat of the 
 auricles, beats synchronously with every second, third, fourth, or more auricular beat. 
 The commonest effect by far, and the one which is most permanent, is that in which the 
 ventricle beats synchronously with every second beat of the auricles ; and, indeed, by 
 careful manipulation of the micrometer screw, it is always possible to bring about this 
 particular kind of rhythm, and in many cases to make the ventricle beat permanently 
 with this rhythm for the rest of the experiment. In other cases this rhythm may last 
 for a considerable length of time, and then the ventricle return to a rate synchronous 
 with that of the auricles. So, too, when the clamp is first tightened the half-rhythm 
 may be caused immediately, or the ventricle may cease to beat for a short time, and 
 then commence to beat with intervals between the beats, corresponding to a large 
 number of auricular beats, such as 1 ventricular beat to 6 auricular ; quickly passing 
 
 JIDCCCLXXXII. 6 M 
 
1000 DR, W. H. GASKELL ON THE RHYTHM OP THE HEART OF 
 
 through such intermediate stages as 1 ventricular to 5 auricular, 1 to 4, 1 to 3, it 
 settles down to the rhythm 1 to 2, at which it remains permanently, or ultimately 
 returns to a rate synchronous with the auricular (Plate 67, fig. 3). 
 
 In some cases the rhythm of the ventricular beats has remained for a long time 
 synchronous with every third beat of the auricles, instead of every second, as in 
 Plate 68, fig. 14, and in other cases, for a shorter time, with every fourth beat. This 
 latter rate of rhythm occurs frequently in the apex of the heart when the clamp is 
 placed across the middle of the ventricle and the beats of the apex and base of the 
 ventricle are compared (see Plate 69, fig. 16) ; here, too, however, the more permanent 
 rate caused by the compression of the clamp is that in which the apex beats synchro- 
 nously with every second beat of the base. 
 
 These facts show that direct compression of the tissue between the motor ganglia 
 and the ventricle causes a certain number of the impulses to be ineffective as far as the 
 causation of a ventricular beat is concerned, although, as shown by the auricular beats, 
 that compression has not interfered with the rate of discharge from the ganglia. 
 Either, then, the compression of the clamp in the auriculo-ventricular groove has 
 caused a diminution in the excitability of the ventricular muscle without altering the 
 strength of the impulses coming to it, or it has diminished the strength of the impulses 
 to the muscle and so caused it to respond to every second instead of to every impulse. 
 Which of these two solutions is the most probable will be better discussed after the 
 consideration of the effects upon the ventricular rhythm of heating the auricles and 
 sinus only, and of the application of poisons to the ventricle alone. 
 
 When by the method described above the auricles and sinus alone are heated, any 
 variations which are noticed in the rhythm of the ventricle must be due to the action 
 of the heat upon the motor impulses before they have reached the ventricular muscle 
 and not to any alteration in the excitability of the muscle itself, for the latter is out of 
 the range of the heating. 
 
 In many respects there is a decided resemblance between the action of the clamp and 
 the effect of heating the auricles and sinus upon the rhythm of the ventricle. Thus, if 
 the heating has been sufficient only shghtly to accelerate and diminish the auricular 
 contractions, then it is found that the ventricle is able to beat synchronously with the 
 accelerated auricular beats, just as a slight compression of the clamp does not interfere 
 with the regular sequence of ventricular upon auricular beats. If the heating continues 
 the auricular beats become weaker and more rapid, and the curves then show that 
 the ventricle is unable to respond with the same rapidity, and ceasing suddenly to 
 beat synchronously with the auricles, it answers with a single contraction to every 
 two contractions of the auricles. When the heating is removed and the auricles 
 begin to beat less frequently,[^the ventricle again alters its rate so as to beat synchron- 
 ously with the auricles with the same suddenness as in its original alteration of 
 rhythm. So, too, an increase in the tightness of the clamp makes the ventricle beat 
 
THE FROG, AND ON THE ACTION OF THE VAGUS NERVE. 1001 
 
 synchronously ^^•itll every second beat of the auricles, and u^Jon loosening the clamp 
 the original sequence of beats returns. 
 
 Finally, in some cases heating the auricles and sinus causes the ventT'icle more or 
 less suddenly to cease beating and remain quiescent in the relaxed condition, although, 
 as will be shown hereafter, we have reason to think that the motor impulses are still 
 passing to the muscle ; similarly, when the clamp in the auriculo-ventricular groove is 
 tightened sufficiently the ventricle remains quiescent, even although there is proof that 
 the impulses have not been entirely prevented from reaching the muscle (see Plate 69, 
 figs. 17 and 18). 
 
 Again, it is to be noticed that when the ventricle is made to beat synchronously 
 with every second beat of the auricles, either by heating the auricles and sinus as in 
 Plate 67, fig. 1), or by tightening the clamp as in Plate 67; fig. 3, the slower contrac- 
 tions are always larger than the previous ones, and this greater force of the contraction 
 is only partly, at all events, due to the fact that with a slower beat the muscle con- 
 tracts from a position of greater relaxation than with a quicker one. The figures, it is 
 true, show that the lever does fall lower between the contractions when the ventricle 
 is beating slowly than when it is beating quickly — a fact which proves that, with the 
 ordinary rate of beating, the ventricle has not time to relax to its full extent before 
 another contraction commences — but they also show that the lever rises above the level 
 of the previous quicker beats ; in other words, the slower beats are accompanied by an 
 increase in the force of the contraction as well as by an increase in the relaxation of 
 the muscle between the beats. 
 
 The similarity between the efiects of clamping and those of heating the auricles and 
 sinus upon the rhythm of the ventricle is so marked and consistent, that we may fairly 
 conclude that any explanation which is sufficient for the one phenomenon must also 
 resolve the other. 
 
 What factors, then, can be conceived as common to these two methods by which 
 such similar results may be produced ? 
 
 In the first place, it may be argued that the excitability of the ventricular muscle 
 has been diminished by the clamping, and therefore the ventricle can only respond once 
 to every two impulses. The possibility of such a causation for the production of the 
 half-rhythm is shown by the fact that curare or muscarin, when applied to the ventricle 
 alone, does ultimately cause that muscle to beat synchronously with every second 
 auricular beat, without any alteration of the rate of the auricular contractions. 
 
 It is, however, to be noticed that these poisons never produce this effect until they 
 have acted so powerfully upon the muscular tissue of the ventricle as markedly to lower 
 the strength of its contractions ; that, in fact, as one would expect, any method by 
 which the excitability of the muscle is lowered to such an extent that it is only able to 
 respond to every second impulse, must at the same time greatly diminish the strength 
 of the contractions of that muscle. 
 
 This fact that a diminution of the contraction force accompanies the production of 
 
 6 M 2 
 
1002 DR. W. H. GASKELL ON THE RHYTHM OP THE HEART OF 
 
 the half-rhythm when it is clearly due to a diminution in the excitability of the ven- 
 tricular muscle, points unmistakably to the conclusion that the half-rhythm caused by 
 clamping, in which, as has been shoAvn, the ventricle contracts with greater force than 
 before the clamp was tightened, is not due to any diminution of muscular excitability 
 caused by the action of the clamp. This is further shown by the following facts : — 
 
 1. The effect of tightening the clamp upon the rhythm of the ventricle is the same 
 in kind, whether the clamp be near the ventricle, as in the auriculo-ventricular groove, 
 or far from it, as at the junction of the sinus and auricles ; i.e., whether the clamp be 
 in a position where it might possibly lower the excitability of the muscle by direct 
 injury, or so far removed as to make it impossible to affect the muscle directly. 
 
 2. When the clamp is placed across the middle of the ventricle the base may continue 
 to beat with the same rhythm as the auricles, while the apex beats synchronously with 
 every second, third, fourth, or more beats of the base ; and it seems impossible to 
 imagine that a direct mechanical injury across the middle of a muscle should so 
 markedly lower the excitability of one side without perceptibly diminishing that of 
 the other. 
 
 3. It frequently happens, as already mentioned, that a standstill of the ventricle 
 occurs immediately upon the clamp being tightened, but that after an interval the 
 ventricle commences to beat again ; if, therefore, the clamp acts by diminishing the 
 excitability of the ventricular muscle, this recommencement of the beats must be due 
 to a gradual recovery of that excitability from the first depressing effect of the 
 increased compression ; this recovery of the excitability ought therefore to be capable 
 of measurement by the method of sending single induction shocks through the muscle 
 at regular intervals, after it has been rendered quiescent by tightening the clamp in 
 the auriculo-ventricular groove. I have made this experiment, and with single shocks 
 sent through every 3 or 5 seconds with the secondary coil carefully regulated so as just 
 to give a contraction at every shock, I could find no evidence whatever that a weaker 
 stimulus was sufficient to produce contractions synchronous with the stimuli, even 
 after a length of time much greater than is ever seen between the time of tightening 
 the clamp and the recommencement of spontaneous beats. 
 
 For these different reasons, then, it is most probable that the compression of the 
 clamp does not alter the rhythm of the ventricle by lowering the excitability of its 
 muscular tissue, and we may infer that the same conclusion holds good in reference to 
 the effect of heating the auricles and sinus. Another explanation must therefore be 
 found. 
 
 Since the experiments of Maeey and others it is recognised as a fact that every 
 contraction of the ventricle is accompanied by a marked diminution of the excitability 
 of the muscle, so that if minimal stimuli be apphed to the ventricle at too rapid a rate 
 the muscle will not be able to contract to each stimulus, because it has not had time 
 to recover sufficiently from the loss of excitability caused by the previous contraction. 
 For this reason, then, we can conceive that any influence like heating the auricles and 
 
THE fhog, and on the action oe the vagus nerv]*;. 1003 
 
 sinus only, which causes tlie motor gangha to send out impulses at a much quicker 
 rate without increasing the excitability of the ventricle, may cause the ventricle to 
 respond synchronously to every second of these quicker impulses, instead of to every 
 impulse. 
 
 Now, although this explanation may be sufficient in the case of the half-rhytbm 
 produced by heating the sinus and auricles only, it is clearly inefficient to explain the 
 action of tightening the clamp, for in this latter case no alteration in the rate of the 
 auricular contractions occurs. 
 
 Since, therefore, the compression by means of the clamp in the sulcus does not 
 produce its effects upon the ventricle by lowering its excitability, or by altering the 
 rate of the impulses from the motor ganglia, it is most probable that it does act by 
 wealcening the strength of the impulses in the same way as suggested by v. Basch, 
 in order to explain the half-rhythm caused by the use of sufficiently weak electrical 
 stimuli. 
 
 Further, the similarity between the effects of tightening the clamp and of heating 
 the sinus and auricles alone, is sufficiently great to suggest that in both cases the 
 effects are produced in the same way, and therefore the main reason why heating the 
 sinus and auricles caused the observed alteration in the rhythm of the ventricle is to 
 be found in the fact that, when the motor ganglia are heated, not only is the rate of 
 discharge of the impulses quickened, but also the quicker impulses are of necessity 
 weaker than before. 
 
 To sum up the conclusions arrived at so far, we have the following propositions : — 
 
 1. The rhythm of the heart is caused by discrete motor impulses passing to the 
 muscular tissue from certain motor ganglia. 
 
 2. Each one of these impulses produces a contraction of the ventricle only when a due 
 relation exists between the strength of the impulses and the excitability of the 
 ventricular muscle. 
 
 3. When each impulse is inefficient to cause a contraction of the ventricle, the 
 ventricular muscle has the power of summing up the effects of two or more of these 
 inefficient impulses, and so continues to beat rhythmically, though no longer 
 synchronously with every impulse. 
 
 4. The easiest explanation of this summation process is as follows : Every impulse 
 which is inefficient to produce a muscular contraction increases the excitability of the 
 muscle, and therefore makes it easier for a second similar impulse to cause a contraction. 
 
 5. The impulses can be made mefficient to produce contractions synchronous with 
 them by lowering sufficiently the excitability of the ventricle, as is seen in the action 
 of poisons, even although the rate and strength of the impulses remain rmaltered. 
 
 6. The impulses can also be made inefficient when the excitability of the muscle is 
 unchanged by diminishing the strength of the impulse, as is seen in the effects of 
 compressing the tissue between the ventricle and the motor ganglia or of heating the 
 auricles and sinus without heating the ventricle. 
 
1004 DR. W. H. GASKELL ON THE RHTTHM OP THE HEART OF 
 
 7. There is a limit to the extent to which a series of inefficient impulses can raise 
 the excitabiUty of the muscle so that the ventricle can remain absolutely quiescent, 
 even although the impulses still pass to it, when those impulses are sufficiently 
 weakened, as will be shown in the second part of this paper. 
 
 The assertion that the rhythm of the heart is normally due to separate impulses 
 discharged from the motor ganglia in the venous sinus, each of which causes a contrac- 
 tion of the cardiac muscle, is not intended to imply that these impulses necessarily 
 travel along simple nerve fibres without passing through one or more interpolated 
 ganglion cells, but only that whatever the nature of the path of the conduction of the 
 nervous impulse may be, separate discharges from the motor ganglia at one end of the 
 path reach the muscle as separate impulses at the other end. 
 
 So, too, I have spoken of the motor ganglia in the venous sinus without meaning 
 thereby to assert that these ganglia may not extend slightly beyond the sinus into the 
 auricular septum as asserted by Lowit'"' (for as a matter of fact experiments which I 
 have made expressly for this purpose have convinced me of the truth of his assertion), 
 or that the other groups of ganglion cells found in different parts of the heart may 
 not upon occasion perform motor functions. 
 
 The whole question of the action of these different groups of nerve cells deserves 
 separate discussion. In this paper I have purposely abstained from that discussion 
 because my object is to describe certain definite well established facts rather than to 
 enlarge upon all the various topics connected with the theory of the heart's action. 
 
 In this first part of the paper, therefore, I have confined myself to the question of 
 the relation of the muscular tissue to the impulses coming to it, and have attempted to 
 prove not only that the normal beat of the heart is dependent upon separate impulses 
 coming to the cardiac miiscle, but that, in addition, the muscular tissue is of such a 
 character that if from any ca\]se the impulses discharged from the motor ganglia 
 should become too weak to cause a contraction, the rhythmical action of the heart can 
 still continue though at a slower rate, because each of these impulses, abortive though 
 it is to produce a contraction, increases the excitability of the muscle, and therefore 
 the latter responds rhythmically to every two or three of the impulses coming to it. 
 
 This relation between the stimulus and the excitability of the muscle, which in the 
 whole heart is to be regarded as a special safeguard for the maintenance of its 
 rhythmical action and not the prime cause of that action, is on the other hand the 
 chief factor in the causation of the rhythm of the isolated apex of the ventricle. 
 
 The large number of investigations on this subject which have been made of recent 
 years may, as far as the rhythm is concerned, be summed up by saying that the 
 muscular tissue of the apex contracts rhythmically under the influence of a sufficient 
 continually acting stimulus, whether that stimulus be electrical, chemical or mechanical. 
 Thus spontaneous rhythmical contractions occur when the constant current or a weak 
 tetanizing current is sent through the tissue, and the rapidity of the rhythm varies 
 
 * Pflugee'h Arcliiv, Bd. xxiii., S. 813. 
 
THE FROG, AND ON THE ACTION OF TEE VAGUS NEKVE. 1005 
 
 directly with, the strength of the current ; also fluids containing different chemical 
 substances, especially alkaline substances like sodium hydrate and sodium carbonate, 
 which according to Biedee]\[ANN'"' increase most markedly the excitability of the 
 striated muscular tissue, produce when supplied to the apex more or less rhythmical 
 contractions. Further, nutritive fluids alone, such as the blood of the animal itself, 
 cause the same effect, provided that in addition a certain pressure exists within the 
 apex cavity ; and the effect of this distension of the walls by pressure, which is the 
 essential jwiiit in this method of producing rhythmical apex contractions, may fairly 
 be classed as a continuous mechanical stimulation. Here, also, according to LuDWiG 
 and LuCHSiNGEE,t the rapidity of the rhytlim varies directly with the extent of this 
 pressure. 
 
 The facts which have just been urged show that the ventricular muscle has the 
 power of summing up the effects of two, three, or more impulses so as to produce a 
 contraction though each of those impulses is inefficieut of itself to cause the muscle 
 to contract. In the same ^vay it is possible to conceive that the muscle should be able 
 to sum up the effects of a series of stimuli which follow one another so closely as to 
 deserve the title of a continuous rather than a discontinuous stimulation. If, then, we 
 have reason to suppose that in the first case the discontinuous stimuli ultimately 
 produce a contraction by increasing the excitability of the muscle, so in the second 
 case we may suppose that a continuous stimulation causes a rhythmical series of con- 
 tractions by acting in the same way. The difference between the two cases would 
 consist in the extent to which the excitability was increased ; in the one, the muscle 
 is not rendered sufficiently excitable to contract without the assistance of a distinct 
 separate stimulus ; in the other, the excitability is increased so much that no separate 
 stimulus is required : the muscle, in fa.ct, can be spoken of as capable of spontaneous 
 contraction. 
 
 PART II. 
 
 On the Action of the Vagus Nerve. 
 
 Ever since the brothers Weber discovered that stimulation of the vagus nerve 
 caused the heart to stand still, physiologists have been incessantly endeavouring to 
 discover the reason of this standstill, with the result that an enormous mass of facts 
 in connexion with the action of the nerve has been accumula'ted, and a variety of 
 hypotheses have been suggested to explain these facts. 
 
 Thus it was found that the vagus at one time causes complete stoppage, at another 
 only slowing of the heart's rhythm ; this fact has led to the view that the complete 
 cessation of beats is simply a prolonged slowing, and therefore that the nerve by its 
 direct action upon the motor ganglia causes the dischai'ges from the ganglia to take 
 place at a slower rate. 
 
 tzungsber. d. k. Akad. d. Wiss. (Wien). Ed. Ixxxii., 1880. 
 t Pfluger's ArcMv, Bd. xxv., S. 211, 
 
lOOG DR. W. H. GASKELL ON THE RHYTHM OF THE HEART OF 
 
 Another view, which largely depends for its support upon the action of various 
 poisons, is, that the nerve does not produce standstill by direct interference with the 
 motor ganglia, but because it excites some inhibitory mechanism which is interpolated 
 between these ganglia and the muscular tissue. Both these views have one hypothesis 
 in common, viz. : that the inhibitory action of the nerve is due to the prevention of 
 the discharges from the motor ganglia from reaching the muscular tissue, and not to 
 the action of the nerve upon the muscle itself In pharmacological literature especially 
 this hypothesis has become so predominant that again and again the statement is 
 made that such and such a poison paralyses or stimulates some part or other of the 
 vagus nerve, when the facts only show in the first case that the vagus is no longer able 
 to produce standstill, and in the second that the poison has by its action caused the 
 heart to beat slower. 
 
 Again, a number of observers, notably Schiff,* have asserted that stimulation of 
 the vagus nerve of the Frog under certain circumstances always causes acceleration 
 of the heart's rhythm, and not slowing : a result which, conjoined with the action of 
 atropia, has led to the supposition that the Frog's vagus contains accelerator as well 
 as inhibitory fibres, and a fresh set of hypotheses has been made with respect to the 
 relative vitality of these two sets of fibres. 
 
 Finally, it has been long known that the contractions which immediately follow the 
 standstill caused by vagus stimulation are much weaker than the normal contractions, 
 and NuELt has shown that stimulation of the nerve weakens, at all events the 
 auricular contractions, even without a preliminary standstill. 
 
 We have, therefore, according to present views at least, three sets of fibres in the 
 Frog's vagus, viz. : fibres which are capable of slowing or entirely preventing the dis- 
 charges from the motor ganglia ; fibres which accelerate those discharges ; and fibres 
 which in some way or other diminish the force of the cardiac contractions. In addition, 
 we have various statements that sometimes only one vagus is active, that at certain 
 times of the year the vagus loses all power, &c. 
 
 The literature of the subject then affords ample evidence of considerable discrepancy 
 not only as to the explanation of the action of the vagus, but also as to observed facts 
 connected with that action. The reason of this confusion will appear in the following 
 pages, and I will say at present that it is based upon a view of the nature of the 
 action of the vagus, which appears to me to be too much one-sided. Too great promi- 
 nence has hitherto been assigned to the action of the nerve upon the motor ganglia — ■ 
 too little to its action upon the muscular tissue. 
 
 The most striking feature of vagus stimulation is a more or less prolonged standstill 
 of the heart. There is no reason d priori to assign this standstill to the action of the 
 nerve upon the rate of the discharges from the motor ganglia rather than to its action 
 upon the muscular tissue of the heart. Either conception is perfectly possible, and its 
 truth can be tested directly by experiment. 
 
 * Pflugbe's Arcliiv, Bd. xviii., S. 172, f Ibid, Bd. ix., S. 83, 
 
THE FROG, AND ON THE ACTION OP THE VAGUS NERVE. 1-007 
 
 Thus if standstill is invariably due to a slowing of the rate of the discharges from 
 the motor ganglia, experiment ought naturally to show that the beats which first occur 
 after the standstill are more infrequent than before the nerve was stimulated, and that 
 the subsequent recovery of the rhythm up to or beyond the original frequency takes 
 place gradually and not abruptly. AIsq a stimulation which is unable to cause complete 
 standstill ought to produce the effect nearest to standstill, viz. : a greater or less slowing 
 of the heart independently of any alteration in the force of the contractions. 
 
 If, on the other hand, standstill is invariably caused by the action of the nerve upon 
 the muscular tissue, so that the latter does not respond to the impulses coming to it, 
 then we should expect to find (in accordance with the law of Bowditch* that the force 
 of the contractions of the ventricle is not dependent upon the strength of the stimulus) ; 
 that the first beats which occur after the standstill are very small, that the force of the 
 contractions gradually increases up to or beyond the orignal force, and that the rate of 
 rhythm after the standstill is not necessarily slower than before the stimulation of the 
 nerve. Also a stimulation which is unable to cause complete standstill ought to produce 
 the effect nearest to standstill, viz.: a more or less marked diminution in the force of 
 the contractions independently of any alteration of rliythm. 
 
 The majority of physiologists have hitherto accepted the first of these views as the 
 invariable explanation of the standstill of the heart caused by the action of the vagus 
 nerve, and in accordance with this view always speak of the vagus as causing inhibition 
 of the heart's action. 
 
 In this present paper I propose to give evidence that, at all events in the heart 
 removed from the body, the second view is the true one, and in accordance therefore 
 with this conception I have throughout spoken of the vagus as causing quiescence of 
 the heart. 
 
 It is of course possible and indeed probable that both these views may be true, 
 and that therefore the vagus may cause standstill sometimes by the one action and 
 sometimes by the other. Whether this is so or not I am not at present able to 
 judge ; I can only say that in the suspended heart I have never as yet seen any 
 reason to suppose that the vagus is capable of producing such a prolonged slowing 
 of the rate of the discharges from the motor ganglia as to entitle that slowing to the 
 name of standstill of the heart ; while on the other hand the quiescence of the heart 
 produced by the action of the nerve upon the force of the muscular contractions may 
 last for a considerable time. 
 
 Again, physiologists and pharmacologists have hitherto considered that the inhibitory 
 action of the nerve is abolished when its stimulation no longer causes standstill or 
 slowing of the heart. This view will clearly require modification if the quiescence of 
 the heart is due to the action of the nerve upon the force of the contractions rather 
 than upon the rate of the discharges from the motor ganglia. Indeed, it will be no 
 
 * Ltjdwig's Arbeiien, 1871, S. 139. 
 MDCCCLXXXII. 6 N 
 
1008 DK. W. H. GASKELL ON THE RHYTHM OF THE HEART OF 
 
 longer possible to speak of the inhibitory action of the nerve apart from its whole 
 action. In every case, then, it Avill be necessary, before we can assert that its action is 
 abolished, to determine that the vagus is no longer able to cause any alteration, not 
 only in the rate of rhythm, but also in the strength of the cardiac contractions. 
 
 I use the term alteration, rather than diminution, of the force of the contractions 
 advisedly, for it will not be sufficient to show that the vagus is no longer able to cause 
 any diminution ; it must also be shown that it is unable to cause any increase of the 
 force of the beats, because, as will be seen, the most permanent and invariable function 
 of the vagus (in the heart removed from the body, at all events) is to increase the 
 strength of the muscular contractions. 
 
 Before describing the results of the experiments upon which the assertions made 
 above are based, it is desirable to say a few words about the conditions under which 
 they were conducted. In every case the vagus nerve was carefully dissected out nearly 
 or quite up to its ganglion and placed on the electrodes, so that there was about a 
 quarter of an inch of free space between the electrodes and the nearest tissue. The 
 experiments were made in the months of February, March, April, May, June, and 
 July of this year, and the animals used were Toads or large, in most cases freshly 
 caught, specimens of Bana temjyojxiria. The left vagus was invariably used, and I can 
 safely assert that in no single instance has its stimulation failed to produce some effect 
 upon the heart, although, as will be seen, that effect is not always the same. 
 
 In my first experiments the heart was suspended by means of Keonecker's forceps 
 attached to the bulbus aortce, the ventricle was slit open from base to apex, and the 
 contractions of the ventricle alone were registered by means of a lever which was 
 attached by a thread to the very apex. The typical effect of valgus stimulation under 
 these circumstances is seen in Plate 67, fig. 4, which shows that by this method 
 complete inhibition can be obtained ; that when the ventricle begins to beat again the 
 first beats are very small, but that they soon begin to increase in size and shortly after 
 the end of the stimulation reach a maximum which is very muchgreater than be for 
 the stimulation. From this maximum the force of the contractions very slowly 
 diminishes to the original size. 
 
 I give this curve simply to show that the nature of the phenomena seen upon vagus 
 stimulation when the clamp is used cannot be ascribed to the use of the clamp, for, as 
 the subsequent curves will show, there is no essential difference between the curves 
 produced whether the clamp is absent or present. As, however, the results are much 
 more interesting when the auricular and ventricular beats are simultaneously recorded, 
 I will proceed at once to describe the effects of stimulating the nerve when the clamp 
 is in the auriculo-ventricular groove and is tightened so as just to hold the tissue ; the 
 ventricle is therefore beating synchronously with every beat of the auricles. 
 
 As the large majority of my experiments have been made with the clamp in this 
 position, I am enabled to draw conclusions from a very great number of curves, each 
 one of which represents a separate stimulation of the vagus nerve. Upon examination 
 
THE FROG, AND ON THE ACTION OF THE VAGUS NERVE. 1009 
 
 of these curves taken as a whole it is seen that althougli stimulation of the vagus 
 produces different effects at different times, these elFecta can all be reduced to the 
 three following types : — 
 
 1. Complete quiescence of both ventricle and auricles, followed by contractions 
 which at first are scarcely visible, but which rapidly increase in size until at the maxi- 
 mum they are much greater than before the stimulation of the nerve ; from this 
 maxinuuu they very gradually decrease until the original force of contraction is again 
 reached (Plate 67; fig. 6, curve B). 
 
 2. During the stimulation no quiescence of either ventricle or auricles, but simply a 
 diminution of the size of the contractions, followed by a rapid and marked augmenta- 
 tion of the contraction curve beyond the original height, and then a slow gradual 
 diminution to the size before the nerve was stimulated (Plate 67, fig. 6, curve A ; 
 Plate 68, figs. 8, 9, &c.). 
 
 3. No primary diminution, but from the commencement of the stimulation the beats 
 increase in force, and after a time gradually return again to the original size (Plate 68, 
 fig. 10). Between these three types every conceivable variation may occur, so that a 
 series of curves may be selected in which no line of demarcation can be drawn between 
 complete primary quiescence, or to use the usual term, inhibition, on the one hand, and 
 a simple primary augmentation of the contraction force on the other. Such a series is 
 to a certain extent represented by Plates 67; 68, figs. 6, B, 6, A, 8, 9, 10. 
 
 Further, the curves show that not only does the height of the contractions vary in 
 a graduated series from the null point on the one side up to a height much greater than 
 before the stimulation on the other, but also that this variation is independent of the 
 rate of rhythm. In the majority of experiments the rhythm is seen to be decidedly 
 accelerated by the stimulation of the nerve, in others no alteration of rhythm can be 
 perceived. Thus in Plate 67, fig. 6, B, as soon as beats appear after the primary 
 quiescence they show a slight acceleration of rhythm; so, too, in such figures as Plate 68, 
 figs. 9, 10, where the nerve stimulation produced a primary diminution and a primary 
 augmentation of the force of the contractions respectively, the rhythm is seen to be 
 accelerated or unaltered from the commencement of the stimulation. 
 
 In all cases where acceleration occurs, the return to the original rate is slow and 
 gradual, in the same way as the return to the original contraction force. 
 
 Another proof that this quiescence, which is caused by stimulation of the vagus, is 
 not due to any interference with the rate of discharge from the motor ganglia, is most 
 markedly shown by the fact that stimulation of the nerve often reduces the ventricle 
 to a state of complete quiescence, while the auricles not only continue beating but beat 
 with greater rapidity than before. Thus we may have complete quiescence of the ven- 
 tricle with the auricles so nearly quiescent that their accelerated contractions are barely 
 visible on the curve (Plate 67, fig. 7), in other cases with the auricular contractions 
 more and more plainly visible (Plate 67, fig. 5), until finally we may obtain curves in 
 which the ventricular beats are diminished down to complete quiescence, while the 
 
 6 N 2 
 
1010 DR. W. H. GASKEILL ON THE RHrTHM OF THE HEART OF 
 
 auricular are, from the commencement of the stimulation, augmented in force (Plate 67, 
 fig, 11). The reverse, however, never occurs — I have never seen quiescence of the 
 auricles with simultaneous primary augmentation in the force of the ventricular 
 contractions. 
 
 A careful examination of the large number of curves which I possess will, I venture 
 to think, afford clear evidence of the truth of the following statements : — 
 
 1. The effect of stimulation of the vagus nerve, which is most constant, is an augmen- 
 tation of the force of the contractions, both of the auricles and ventricle; an 
 augmentation which cannot be regarded as a mere rebound, so to speak, from a 
 previous diminution of the force of the contractions. 
 
 2. In the case of both auricles and ventricle a series of curves can be obtained 
 which show that stimulation of the vagus is able to produce a perfect gradation of 
 effects upon the strength of the contractions irrespectively of the rate of rhythm : a 
 gradation which extends from a simple augmentation of the force of the contractions 
 as the result of the nerve stimulation, down to so great a primary diminution of that 
 force that the contractions are no longer visible, and therefore quiescence results from 
 the stimulation of the nerve. 
 
 3. The auricles and ventricle maybe in different phases of this gradation at the same 
 moment, with the quahfication that, if quiescence be called the lowest and primary 
 augmentation of the force of the contractions, the highest term of the series, the 
 ventricle, is always in a lower phase than the auricles. 
 
 The auricular curves are different from the ventricular in one or two other details ; 
 thus the maximum effect on the force of the contractions is reached more quickly after 
 the end of the stimulation in the former than in the latter, so that the auricular beats 
 have already reached their maximum, while those of the ventricle are stiU increasing. 
 (Plate 68, figs. 9, 10). The auricles also return to their original force of contraction 
 much more quickly than does the ventricle ; as is seen in Plate 68, figs. 9, 10. The 
 same figures show another peculiarity of the auricular curves, which is especially 
 characteristic of the Toad's heart, viz. : after the maximum force of contraction has been 
 reached, the contractions gradually diminish to a height less than before the stimulation, 
 and then again increase up to or slightly beyond their original height : a peculiarity 
 which I have never as yet observed in the ventricular curves. 
 
 I have already said sufficient to justify the assertion which I made above, that the 
 vagus is never absolutely inefficient ; it always produces some effect or other upon 
 stimulation, and I have described a variety of the effects which it does produce. 
 Hitherto I have considered the curves as a whole, and have shown that the different 
 effects seen when the nerve is stimulated — as far at least as the action of the nerve 
 upon the force of the contractions is concerned — can all be arranged in a graduated 
 series in which no line of demarcation can be drawn separating one especial effect 
 from another. It remains to be seen whether a similar gradation can be produced 
 
THE FROG, AND ON THE ACTION OF THE VAGUS NERVE. 1011 
 
 by a series of stimulations in each separate experiment, and, if so, what conditions are 
 necessary for its production. 
 
 In the first place, stimulation of the vagus is much more hkely to reduce the force 
 of the contractions down to complete quiescence immediately after removal of the heart 
 from the body, than after it has been suspended for some time ; and, indeed, a variety 
 of facts can be brought together which all point in one direction, viz. : that the produc- 
 tion of quiescence by stimulation of the nerve stands in intimate relation with the 
 existence of a suitable nutrition of the heart. Thus it frequently happens that typical 
 inhibition can be obtained before the heart is removed from the body, although after 
 it has been suspended it is impossible by any strength of stimulation to reduce the 
 strength of the contractions to such an extent as to cause standstill. 
 
 Again, expeiiments made in June for this express purpose show that if the heart be 
 suspended as quickly after removal as possible, and the circulation be kept intact till 
 the last moment, then, with a certain strength of current the first stimulation caused 
 absolute quiescence ; the next, although of the same strength and length, only a primary 
 diminution of the force of the contractions, and with succeeding stimulations of the 
 same strength and the same length and following upon one another at as nearly as 
 possible the same intervals of time, there was a decided tendency for the primary 
 diminution of the contraction force not only to diminish in extent, but also to affect a 
 smaller number of beats, until at last the stimulation caused an increase in the force of 
 the contractions with a previous diminution of only one or two or even no beats at all 
 (see Plate 68, fig. 9). 
 
 Indeed, it can be said that in the course of each separate experiment the successive 
 stimulations of the nerve tend to show the same gradation of effects from complete 
 quiescence followed by augmentation on the one hand, up to a simple primary augmenta- 
 tion of the force of the contractions on the other, as has already been pointed out 
 from the consideration of the whole number of curves. 
 
 In the second place, the examination of my curves indicates that the nature of the 
 special nutritive condition of the heart, upon which the phenomenon of vagus standstill 
 depends, may possibly be given by the chemical examination of a large number of 
 hearts at different times of the year, for as far as I can judge from this first series of 
 experiments, standstill is more likely to occur upon vagus stimulation, after the heart 
 has been cut out and suspended, in the early spring months of the year than in the 
 summer months. Indeed, in some cases in March, stimulation was still able to cause 
 quiescence even after the heart had remained suspended for nearly two hours. 
 
 In Plate 68, fig. 12, curve A, I give an example of quiescence of the auricular contractions caused by 
 vagus stimulation, which was obtained about an hour and a half after removal of the heart from the body, 
 during which time the vagus had been stimulated nine times. In curve B of the same figure, which is a 
 continuation of curve A (except that between A and B the vagus was stimulated so that the beats at the 
 commencement of the curve B represent the maximum contractions due to that stimulation) the vagus 
 was stimulated with the same strength of current at frequent intervals, so that the auricle was not 
 allowed to reach the maximum of its contractions. The curve shows well not only that quiescence was at 
 first produced, but also the resolution of that quiescence into barely visible rhythmical contractions. 
 
1012 DR. W. H. GASEELL ON THE RHYTHM OP THE HPJART OP 
 
 From these experiments the conclusion can be drawn that the impairment of the 
 nutrition of the heart caused by the removal of the circulation is not of itself sufficient 
 to take away from the vagus the power of reducing the force of the contractions to the 
 null point ; but rather that, in addition, some unknown factor, upon which this diminu- 
 tion of the beats depends, is more powerful at one time than at another. 
 
 In all that has been said hitherto, no evidence has been given that the vagus is able 
 to cause any slowing of the rate at which impulses are discharged from the motor 
 ganglia, but, on the contrary, clear evidence that it is able to accelerate that rate, and 
 although the large majority of my curves point directly to that conclusion, yet occa- 
 sionally a curve is obtained in which an undoubted slowing has taken place. In some 
 cases it is possible that the slowing may be due to the failure of certain impulses to 
 produce a contraction as is undoubtedly the case in the slower ventricular beats seen 
 in Plate 69, fig. 15, where the stimulation of the vagus caused the ventricle to beat for 
 a time synchronously with every second auricular beat. On the other hand, such 
 slowing as is seen in Plate 67, fig. 13, where the recovery of the rate of rhythm after 
 the end of the stimulation was gradual both in auricles and ventricle, cannot be 
 explained, except upon the supposition that the nerve stimulation had slowed the rate 
 of the discharges from the motor ganglia. 
 
 Indeed, the fact that the vagus is able to cause a slowing of the heart s rhythm is so 
 well established as not to admit of doubt ; all I contend for is, that that slowing is not 
 always a sufficient explanation of the phenomenon known as vagus inhibition. 
 
 Further, I venture to suggest that the hypothesis that the Aagus contains two sets 
 of fibres going to the motor ganglia, of which the one causes upon stimulation accelera- 
 tion, the other a slowing of the rate of discharge from the motor ganglia, is no more 
 necessary than the similar supposition that the nerve contains two sets of fibres sup- 
 plying the muscular tissue, of which the one causes a diminution, the other an increase 
 of the force of the contractions. 
 
 The experiment from which Plate 67, fig. 13, is taken shows clearly the rapid diminution of the power 
 of the vagns to produce a slowing of the heart when the heart is removed from the body, and suggests 
 that that removal affects the action of the nerve upon the rate of rhythm in the same direction as it 
 affects its action upon the force of the muscular contractions. Thus, in Plate 67, fig. 13, the effect of the 
 first stimulation of the nerve immediately after the heart was suspended, is given. The second stimalation, 
 about a minute after the first, still caused a decided slowing, but very much less marked in extent than 
 before. The third stimulation showed that the nerve was no longer able to produce any slowing, although 
 the effect upon the force of the contractions was as great as in the previous stimulations. 
 
 On the injluence of the vagus nerve upon the excitability of the ventricular muscle. 
 
 Seeing that the vagus acts so powerfully upon the force of the muscular contract 
 tions, it is natural to expect that it also has an influence upon the excitability of the 
 muscular tissue. The nature of this influence can be determined by the following 
 considerations. 
 
THE FROG, AND ON THE ACTION OE THE VAGUS NERVE. 1013 
 
 In the first part of this paper I have attempted to prove that the ventricle beats 
 synchronously with the a\u'icles when a due relation subsists between the strength of 
 the impulses from the motor ganglia and the excitability of the ventricle. When, 
 however, the strength of the impulses is diminished either by clamping or by the 
 action of heat upon the motor ganglia, this due relation is destroyed and the ventricle 
 either beats synchronously with every second, third, or more contractions of the 
 auricles or else does not beat at all. If under these circumstances the excitability of 
 the ventricular muscle be increased, then the relation between the strength of the 
 impulses and the muscular excitability, which is necessary for synchronous contractions, 
 will be restored, eitlier fully or partially, according to the extent to which the 
 excitability is raised. On the other hand, if the excitability be lowered then that due 
 relation will be still further destroyed, and each beat of the ventricle will follow upon 
 a still larger number of auricular beats than before. 
 
 In accordance with this method of testing the excitability, experiment proves that 
 the vagus may cause a diminution of the excitabilitj'' of the ventricle during the first 
 part of its action, during, therefore, the period when it is known to diminish the force 
 of the contractions ; and may cause an increase of excitability v?hen it augments the 
 force of the contractions. 
 
 I will now proceed to give the facts upon which the truth of this proposition 
 depends, and will first examine the action of the nerve when the clamp in the auriculo- 
 ventricular groove is tightened so as to make the ventricle beat synchronously with 
 every second or third beat of the auricles. 
 
 In this case the rnost striking effect of stimulation of the nerve is the alteration 
 which is produced in the rate of the ventricular rhythm rather than the variations in 
 the force of the ventricular contractions. It is true that the nerve stimulation may 
 still cause the force of the ventricular contractions to be diminished and augmented 
 in the same way as already described, but neither the diminution nor the augmentation 
 are so manifest as when the ventricle is beating synchronously with every auricular 
 beat ; this is doubtless largely owing to the greater size of the ventricular contractions 
 in consequence of their slower rate of rhythm. This is, however, not the main 
 distinction between the two cases. 
 
 When the ventricle is beating synchronously with every beat of the auricles we have 
 seen that this synchronism continues during the period of diminution as well as during 
 the period of augmentation of the force of the contractions ; when, however, the 
 ventricle is beating synchronously with every second beat of the auricles the same law 
 does not necessarily hold ; in many cases stimulation of the nerve causes a sudden 
 alteration in the relation of the ventricular to the auricular rhythm. 
 
 In the first place the rhythm of the ventricle becomes synchronous with that of the 
 auricles for a longer or shorter period. This period of synchronism corresponds to the 
 time when the contractions would have been greatest if the ventricle had been beating 
 in due sequence with the auricles ; it may therefore occur sometimes during the stimula- 
 
1014 DR. W. H. GASKELL ON THE RHYTHM 0¥ THE HEART OF 
 
 tion, at other times some considerable time after the end of the stimulation. Thus in 
 Plate 68, fig. 14, the ventricle was beating synchronously with every third beat of 
 the auricles ; for a definite period after the end of the stimulation of the vagus its 
 rhythm was changed so that it beat synchronously with every second instead of with 
 every third auricular beat. Similar figures might be given to show how the vagus 
 causes the ventricle to beat synchronously with every beat of the auricles instead of 
 with every second beat. 
 
 These curves show that stimulation of the vagus increased the excitability of the ven- 
 tricle sufficiently to enable it either wholly or partially to recover for a time the normal 
 sequence of its beats upon those of the auricles, and also that increase of excitability 
 took place at the same time as the maximum increase in the force of the contractions. 
 
 In the second place, stimulation of the vagus may cause a primary slowing of such a 
 character that a variable number of auricular beats are dropped out from the ventricular 
 curve, and then afterwards the ventricle may regain its original rhythm or even become 
 synchronous with every beat of the auricles (Plate 69, fig 15). 
 
 Further, this slowing of the ventricle may not only be coincident with an acceleration 
 of tlie auricles, but in fact is more likely to occur when stimulation of the nerve causes 
 a marked auricular acceleration. This, at first sight paradoxical, assertion follows neces- 
 sarily upon the arguments put forward in the first part of this paper, if it be assumed 
 that the vagus diminishes the excitability of the muscle at the same time that it 
 depresses the strength of the contractions ; for the greater rapidity of the auricular 
 contractions denotes not only quicker but also weaker impiilses from the motor ganglia ; 
 and it is clear that, if the impulses be weakened at the same time that the excitability 
 is lessened, a larger number of impulses will require to be summed up in order to 
 produce a contraction, than if the excitability only is diminished. 
 
 Again, if the clamp be placed across the middle of the ventricle, and the contractions 
 of the base and apex of the ventricle be registered, the same diminution of excitabihty 
 can be observed. Thus, when the apex is beating synchronously with every second or, 
 as in Plate 69, fig. 16, with every fourth beat of the base, then coincident with the 
 diminution and acceleration of the contractions of the base, which occur during the 
 stimulation of the nerve, the beats of the apex take place at a slower rate than before, 
 because each apex contraction corresponds to a lai-ger number, and therefore probably 
 to a longer series of base-contractions than before the stimulation. 
 
 Thus in the instance given (Plate 69, fig. 16) I have marked the corresponding contractions on the two 
 sides with the same numbers, and it is seen that before the stimulation of the vagus the relation between 
 the rhythm of the apex and the base was such that each apex-contraction corresponded to four base- 
 contractions. During the stimulation the beats of the base became weaker and more frequent, while 
 those of the apex were so much slower that only two beats took place, of which the first corresponded to 
 twelve beats of the base and the second to eight beats. After the stimulation the original relation between 
 the rhythm of the apex and base was restored, so that each apex- contraction again corresponded to four 
 base-contractions. Curves similar to this are those most frequently obtained with the clamp in this 
 position. 
 
THE FROG, AND ON THE ACTION OF THE VAGUS NERVE. 1015 
 
 These facts alone make it probable that the vagus lowers the excitability of the 
 muscle at one time and increases it at another. Now although this diminution of 
 excitability occurs at that period of the vagus action when the stimulation of the 
 nerve is known to cause a diminution of the force of the contractions, yet it is clear 
 that the connexion between the two is relative and not absolute. As has been seen, 
 when the contractions are synchronous with the impulses, stimulation of the nerve is 
 able to reduce the force of the contractions to the vanishing point, and yet up to the 
 last moment of visible contractions every impulse is followed by a contraction — i.e., the 
 excitability does not in this case fall sufficiently, in relation to the strength of the 
 impulses, to prevent the muscle from responding to every impulse, even although the 
 contractions become so small as to be almost invisible. Since, therefore, we have 
 reason to siippose that the vagus stimulation does diminish the excitability at the 
 first period of its action- — i.e., at the time when it diminishes the force of the con- 
 tractions — and yet leaves the cardiac muscle still able to respond synchronously to 
 the impulses, provided that the latter have not been diminished in strength, the 
 inevitable conclusion is, that normally the excitability of the muscular tissue is greater 
 than is necessary to enable it just to respond to every impulse. In other words, 
 a range is allowed within which the excitability may fluctuate without thereby 
 preventing the synchronous response of the muscle to the impulses, as long as the 
 strength of the impulses does not diminish. As a rule the lower limit of this range 
 is not passed, in consequence of vagus stimulation, when the strength of the impulses 
 is not interfered with ; and therefore in these cases the diminution of excitability 
 caused by the vagus is not rendered visible. This diminution can, however, be made 
 manifest by first reducing the excitability of the muscle to some extent. Thus if 
 muscarin be applied to the ventricle alone, when it is beating synchronously with 
 every beat of the auricles, and the vagus be stimulated when the muscarin has, 
 without altering the synchronism, greatly reduced the force of the ventricular contrac- 
 tions, then the stimulation may cause the ventricle to beat synchronously with every 
 second auricular beat for a short period, showing that the stimulation of the nerve, 
 added to the effect of the muscarin, has reduced the excitability of the ventricle to a 
 gj'eater extent than the muscarin alone had done. 
 
 Hitherto I have chiefly spoken about the diminution of excitability caused by the 
 vagus, and will therefore now proceed to give further proofs that the vagus increases 
 the excitability of the muscle at the same time that it augments the force of its con- 
 tractions. The most striking proof of this fact, in addition to what has been already 
 said, is given by the effect upon the ventricle of stimulation of the nerve when the 
 ventricle is rendered quiescent either by heating the sinus and auricles or by tightening 
 the clamp in the auriculo-ventricular groove. 
 
 In both cases the effect is the same, and is well exemplified in the series of Plate 69, 
 fig. 17, curves A, B, C, D, which represent the effects of vagus stimulation in a single 
 
 MDCCCLXXXII. 6 
 
1016 DR. W. H. GASKELL ON THE RHYTHM OF THE HEART OF 
 
 heating experinient. Plate 69, fig. 18, shows the corresponding effect -when standstill 
 is produced by clamping. 
 
 A consideration of these and similar curves shows that when, whether from the 
 effect of clamping alone or from the combined effects of heating the motor ganglia 
 and clamping, the ventricle is not beating, stimulation of the vagus causes a series of 
 ventricular beats which commences as a rule some little time after the end of the 
 stimulation. These contractions last for a certain time, and then the ventricle again 
 becomes quiescent, until, with a new stimulation of the nerve, a new group of con- 
 tractions is produced. Again, the contractions in each of these series are synchronous 
 with the auricular contractions, and are strong vigorous contractions such as would 
 have been produced had the ventricle been beating when the nerve was stimulated. 
 This shows that the beats in each of these series, as far as their mere occurrence 
 is concerned, are due to motor impulses which pass to the ventricle at the same 
 rate as to the auricles, and therefore that during the previous quiescence the motor 
 impulses were still passing to the ventricle, but were not a,ble to produce any con- 
 tractions. Again, these series of contractions do not as a rule take place during 
 the stimulation of the nerve, but some time after the stimulation, and the position 
 of each series corresponds closely to the position of the maximum contractions seen 
 after the end of the stimulation of the nerve in the ordinary curve of vagus stimu- 
 lation. An explanation, therefore, of this action of the vagus is clearly given by 
 the supposition that by the action of the nerve the excitability of the ventricular 
 muscle is increased at the same time that the force of the contractions is increased. 
 Hence as soon as the excitability is sufBciently raised the motor impulses which have 
 been rendered inefficient by the action of the clamp, or by the action of heat upon the 
 motor ganglia, are able to cause contractions : and these contractions last until by 
 the passing off of the vagus influence the excitability has again sunk too low for 
 the impulses to be able to cause a contraction. 
 
 The beats in each series are not necessarily synclironous with every impulse from the beginning to the 
 end of the series. As far as I have seen they are usually synchronous in the middle beats of each group, 
 but the series may begin and end with one or two beats which are synchronous with every second auricular 
 contraction instead of with every one. This latter form of curve simply denotes that the rise and fall of 
 the excitability has not been so abrupt as in the first case, as can easily be seen by drawing a diagram to 
 represent the curve of excitability in relation to the strength of the impulses. 
 
 Further, it was noticed in the course of the experiment from which Plate 69, fig. 17, is taken, that 
 after a while the same strength of stimulation caused a series of ventricular contractions when the 
 auricles and sinus were not heated, and no effect whatever when the nerve was stimulated during 
 the time of heating ; in other words, when the strength of the impulses was made still weaker by the 
 heating, the rise of excitability caused by the vagus stimulation was not sufficient to make those impulses 
 efficient to cause ventricular contractions. 
 
 Also (as is seen in Plate 69, fig. 17, B, 0, D) during the course of the experiment each series of 
 ventricular contractions lasted on the whole a shorter and shorter time, and commenced later and later 
 after the end of the stimulation — a fact which is to be explained by the progressive exhaustion of the 
 whole heart. 
 
THE FROG, AND ON THE ACTION OF THE VAGUS NERVE. 1017 
 
 On the action of the vagus upon the ventricular muscle when that muscle is beating with 
 
 alternately strong and loeak heats. 
 
 When the heart is suspended in the manner already described and the ventricle is 
 beating in due sequence with the auricles, it frequently happens that, although the 
 auricular contractions are all equal in force, the ventricle is seen to be beating with 
 alternately Aveak and strong contractions, as is shown in Plates 67, 69, figs. 7, 19, 21. 
 If, now, the vagus be stimulated, this alternation in the size of the ventricular contrac- 
 tions disappears simultaneously with the increase in the force of the contractions caused 
 by the nerve stimulation, and reappears again as the contractions return to their 
 original size ; and if the nerve be stimulated a second time, while the contractions are 
 still equal in force, then with the primary diminution in force caused by the stimula- 
 tion the alternately weak and strong beats again appear, and again give way to beats 
 of equal force with the subsequent augmentation of the force of the contractions. This 
 is well shown in Plate 69, fig. 19. 
 
 It is difficult to come to any final conclusion upon the causation of this alternation 
 in the strength of the ventricular contractions, though it is possible to somewhat limit 
 the area of discussion. In the first place, they are clearly local in origin, for by clamp- 
 ing across the middle of the ventricle the same alternation in strength is sometimes 
 seen in the beats of the apex, while those of the base of the ventricle remain of the 
 same strength throughout (Plate 69, fig. 20). Here, too, the vagus removes this 
 alternation in the same way as in the case of the whole ventricle. Also, as far as I 
 have seen, this phenomenon is confined to the ventricle. I have never seen any 
 appearance of this alternation of contraction-force in the auricular beats. In the second 
 place, they are not necessarily due to the clamp, for the same alternation may occur 
 when the ventricle alone is suspended and no clamp is used. 
 
 Further, the sizes of these alternately weak and strong contractions are clearly 
 dependent upon each other, so that, other things being equal, the more marked the 
 diminution in the weak contractions the more marked also is the increase in the strong 
 ones which alternate with them ; therefore if, as sometimes happens, the alternation 
 disappears, temporarily though it may be, when the ventricle is moistened with normal 
 sahne solution, then the size of the equal contractions is intermediate between the 
 size of the alternately weak and strong ones. This relation is beautifully seen when, 
 as is apt to occur, a secondary rhythm appears in these contractions, as is shown in 
 Plate 69, fig. 21. Here it is seen that the weak contractions increase to a maximum 
 while the strong contractions diminish simultaneously to a minimum, and vice versa, the 
 minima of the weak correspond to the maxima of the strong. 
 
 Now we know from the experiments of BowDlTCH* that the force of the ventricular 
 contractions is independent of the strength of the stimulus. The explanation, there- 
 fore, of this alternation in the force of the contractions must be sought for in the 
 
 * Op. cit. 
 6 o 2 
 
1018 DR. W. H. GASKELL ON THE RHYTHM Oi^ THE HEART OF 
 
 muscular tissue itself, and it seems to me that the most probable explanation is that a 
 larger amount of tissue contracts when the beats are large than when they are small, 
 and that, therefore, in all probability, certain portions of the ventricle respond only to 
 every second impulse, whUe other portions respond to every impulse. The obsers^a- 
 tions of AuBERT * show that by the direct action of a blow a circumscribed area of the 
 ventricular muscle can be made to remain quiescent, while the rest of the ventricle is con- 
 tracting rhythmically. I am inclined, therefore, to suggest that, owing to some cause in 
 the manipulation, such as cutting open the ventricle, or some other cause which affects 
 the ventricle unequally, the excitability of the ventricular muscle is at the time not 
 absolutely the same throughout, so that, although the impulses remain the same in 
 strength, yet certain parts which possess a lower excitability are able to respond only 
 to every second impulse, whUe the rest of the tissue responds to every impulse. In 
 this way, if the strength of the contractions depends upon the amount of tissue con- 
 tracting, we see not only that every second beat must be larger, but also that the size 
 of each strong contraction must vary inversely as the size of each corresponding weaker 
 contraction. 
 
 Upon this assumption the action of the vagus admits of easy explanation, for it is 
 evident thaij the alternation disappears during the time when we have reason to sup- 
 pose that the maximum rise of excitabUity caused by vagus stimulation is produced, and 
 reappears when the normal excitabihty is regained, or when the excitability is lowered 
 below the normal by the action of tlie vagus. If, therefore, we look upon this alterna- 
 tion in the strength of the contractions as due to a local lowering of excitability, so 
 that certain portions contract once only to every two contractions of the rest of the 
 ventricle, then it is clear that as soon as the excitability of these parts is raised suf- 
 ficiently for them to respond to every impulse, every contraction must become as 
 strong as every other contraction, for every part of the ventricle will contract to 
 every impulse. On the other hand, if the general excitability is lowered there must be 
 a greater tendency for this alternation to occur ; thus, it sometimes happens that when 
 the ventricle is beating with contractions of equal height, stimulation of the vagus 
 causes not only a lowering of the height of the contractions, but also a temporary 
 appearance of alternately strong and weak beats. 
 
 Also, when there is a great difference in size between the consecutive contractions, 
 it is possible for the stimulation of the vagus to fail in increasing the excitability of all 
 portions of the ventricle to an extent sufficient to cause them to respond synchronously 
 with every impulse, so that the alternation does not entirely disappear in any part of 
 the curve, although the diflFerence in height between consecutive beats is not so great 
 during the period of augmentation of the force of the contractions as before the stimu- 
 lation ; in other words, the nerve stimulation has sufficiently increased the excitability 
 of some portions of the affected area, though not of the whole of it. 
 
 * Pflugee's Arehiv, Bd. zxiv., S. 357. 
 
THE FROG, AND ON THE ACTION OF THE VAGUS NERVE. 1019 
 
 On the action of the vagus nerve upon the tonicity of the heart. 
 
 The question whether any particular influence upon the heart causes the relaxation 
 of the tissue to become greater or less than the normal, is always attended with the 
 difiiculty that it is impossible to say what the normal amount of relaxation really is. 
 Thus with the ordinary rate of rhythm the amoimt of relaxation is always greater with 
 a slower beat than with a quicker one, a fact which is to be explained by the simple 
 supposition that the condition of contraction has not absolutely passed away when the 
 next contraction takes place unless the contractions follow at a slower rate than the 
 normal ; so that for tliis reason alone a greater relaxation must occur if the vagus causes 
 a slowing of the beats and a less relaxation if the beats are made more frequent. On 
 the other hand, if the tissue is relaxed when the rhythm of the beats is accelerated or 
 unaltered, we may then fairly speak of an increased relaxation of the tissue, and if the 
 relaxation is less, when the rate is the same or slower, then we may speak of a 
 diminished relaxation of the tissue. Thus, for instance, every experiment shows that 
 muscarin and lactic acid truly increase, while sodium hydrate and digitalin truly diminish 
 the normal relaxation of the tissue. 
 
 Now in endeavouring to estimate the extent of relaxation in a hollow muscle like the 
 ventricle, it is clear that the measurement of its capacity will afford a better chance of 
 obtaining a visible amount of relaxation than any mere linear measurement such as 
 is given by the method described above. I have therefore endeavoured to find out 
 whether the vagus really causes any relaxation of the ventricle by the following 
 method : — 
 
 The instrnment wHob. I have used is a modification of Roy's tonometer* and is represented in Plate 70, 
 figs. 22, 23. The glass chamber A is in connexion by means of a metal tnbe with the recording chamber B, 
 to the lower end of which the membrane used by Rot is tied and within which the piston attached to this 
 membrane is able to move up and down and so to canse corresponding movements of the lever. The 
 funnel and tap on the top of the metal chamber B is for the purpose of filling this chamber and the con- 
 necting tnbe C with oil. The tap in the tnbe C enables ns to free this tnbe from air ; and somewhat below 
 the middle of the chamber B is a tap which allows oil to be drawn out of the apparatus by means of the 
 indiarubber tube D, and so to exhaust the pressure within the whole apparatus and raise the lever to the 
 horizontal position as described by Roy in the original description of his tonometer. The glass chamber A 
 is provided with a vulcanite stopper which fits absolutely tight, so that any variation in the contents of 
 the chamber A must be transmitted to the chamber B through the tube C, and cause a corresponding 
 variation in the position of the lever. There is no necessity that the chamber A should be filled with oil ; 
 it may be filled with normal salt solution or any other fluid without preventing the working of the mem- 
 brane, because the lower extremity of the chamber B is on the same level with the top of the chamber A, 
 and therefore the oil in the chamber B will not be contaminated by the salt solution in A. 
 
 The vulcanite stopper, of which a separate drawing is given on Plate 70, fig. 23, contains five holes of exactly 
 the same diameter ; small portions of a piece of metal tubing which has been ground accurately to fit these 
 holes can be inserted into one or more of them, according to the requirements of each experiment, and those 
 
 * Journal of Physiol., vol. i., p. 452. 
 
1020 DR. W. H. GASKELL ON THE RHYTHM OF THE HEART OF 
 
 holes which are not required can be closed absolutely by vulcanite pings, of which one is represented in the 
 drawing. 
 
 Different instruments can be fixed into any of these pieces of metal tubing, and so the apparatus be made 
 available for a variety of experiments, either upon the whole heart or on the ventricle or apex alone. 
 
 In the figure the vulcanite stopper is represented when fitted up for the purpose of investigating the 
 action of the vagus nerve upon the whole heart when an artificial solution of blood is flowing into it. 
 
 The metal cannula E, which fits tightly into any one of the pieces of metal tubing, is tied into the com- 
 mencement of the venous sinus — the small glass cannula in the middle is fixed into one of the aortic trunks ; 
 the plate F is a cork plate fixed on a piece of thin metal, which is soldered to its corresponding piece of 
 metal tubing. This piece of tubing can either be sealed hermetically or be left open and attached to a 
 manometer, in order to observe the pressure within the apparatus. The glass tube G, which is hermetically 
 sealed at both ends, carries within it a pair of platinum electrodes, bent at their extremities into the form 
 of a loop. Two very small holes are blown exactly opposite to each other in the middle of this tube, and 
 the electrodes are fixed within it so that the line joining the two holes is just below the lowest point of the 
 electrodes. Through these holes the vagus nerve can be drawn by a thread attached to its extremity, and 
 by pinning the end of the thread on to the cork slab F, the nerve will remain always in contact with the 
 electrodes. Since the glass tube which contains the electrodes is closed both above and below, the air 
 within it does not escape, and therefore the part of the nerve which lies on the electrodes is during the 
 whole time of the experiment surrounded by air, although the heart itself is plunged in normal salt solution. 
 In this way all escape of current is avoided. 
 
 While the heart is still within the body the arterial cannula is tied into the right aortic trunk, and the 
 metal venous cannula into the commencement of the venous sinus (this cannula has an internal diameter 
 of fully 3 millims.). The two superior venas cavee are tied without injuring the vagus nerve on the left 
 side, the roots of both lungs and the left aortic trunk are ligatured, the lungs are out away, and the heart 
 with the left vagus intact is removed from the body. The cannulee are then filled with blood solution and 
 slipped on to their respective pieces of metal tubing ; the heart is fixed in its place by means of pins stuck 
 through the oesophagus and surrounding tissue into the cork slab F. The vagus nerve is then gently 
 drawn through the glass tube over the electrodes and fixed by means of a pin through the thread attached 
 to its extremity. 
 
 The vulcanite stopper is now placed in position in the chamber A, and the superfluous salt solution 
 allowed to escape through that hole, which is afterwards closed by the vulcanite plug, as shown in the 
 figure. The oil is now allowed to run out of the indiarubber tube D until the lever is horizontal, and the 
 tracing can then begin. 
 
 The arrangement for keeping constant the pressure of the fluid sent into the heart is the same as already 
 described in my former paper.* When the lever is made horizontal by the running out of the oil, it is 
 found that the negative pressure in the chamber A amounts to 5 centims. of water. Therefore the pressure 
 of the fluid in the venous side of the heart is 5 centims. of water, when the level of the blood solution is 
 the same as that of the extremity of the cannula in the venous sinus. 
 
 The curves obtained by this method (Plate 70, fig. 24) are sufficiently striking, but 
 unfortunately not easy to interpret. From the nature of the arrangement it is clear 
 that the beats in the curves represent the changes in volume of the whole heart when 
 beating with a blood supply at a constant pressure. Therefore when the auricle contracts 
 that contraction ought not to be registered at all, for it causes simply a transference of 
 fluid from one part of the heart to another, unless by the contraction a certain amount 
 of fluid is thrown backwards along the inflow tube. Again, when the ventricle 
 
 * Op. cit. 
 
THE FROG, AND ON THE ACTION OF THE VAGUS NERVE. 1021 
 
 contracts the curve registers not the amount of fluid thrown out by that contraction, but 
 the difference between that amount and. the amount which has flowed into the auricles 
 during the time of that contraction ; and this latter amount will depend upon the 
 extent to which the auricles have completed their relaxation when the ventricle begins 
 to contract. It seemed to me, therefore, impossible to come to any satisfactory conclu- 
 sions when auricles and ventricle were both beating. In consequence, I have attempted 
 to prevent the auricles from beating by raising the pressure of the blood solution 
 flowing into them sufficiently high, and as RoY''^ has asserted that a pressure of 
 15 centims. is almost sufficient to prevent their contracting, I have always used 
 a higher pressure than this, and have always carefully observed that there were no 
 movements of the auricles visible to the naked eye or registered on the tracing before 
 I proceeded to stimulate the vagus nerve. In this way I have seen most distinct 
 relaxation of the ventricle upon vagus stimulation without any slowing of the rate 
 of rhythm. Thus Plate 70, figs. 25 A and B, represents two cases taken from the 
 same heart as fig. 24 ; the pressure within the auricles was 28 and 29 centims. of 
 water respectively, and as is seen by the gradual slope of the curve in fig. 25 B as a 
 whole, there was a sKght amount of leakage from some part in consequence of the 
 high pressure ; still the curves show clearly enough that the contractions which occur 
 when the nerve is stimulated start from a lower level of the lever ; and as no variations 
 in the condition of the auricles was to be noticed, it seems to me that the only 
 explanation of such curves as these is that the vagus causes a true relaxation of the 
 muscular tissue of the ventricle, and in all probability of the auricles as well. 
 
 If, now, we turn to the consideration of the curves obtained by tbe method of suspending the heart, we 
 see decided indications of the same fact ; in many of the curves it can be noticed that with the diminution 
 of the beats caused by vagus stimulation, the diastolic line formed by joining the points of greatest 
 relaxation falls very slightly nearer to the abscissa than before the stimulation (Plate 69, figs. 15, 17 A, &c.). 
 
 Another peculiarity can be seen in many of these curves, which is sometimes much more pronounced 
 than at other times, viz. ; that with the increase in the force of the contractions, the diastolic line is raised 
 higher above the abscissa ; this is well shown in Plates 68, 69, figs. 10 and 17 A. This diminution of 
 relaxation between the beats may be due to an increased touicity of the ventricle, coincident with the 
 increase in the force of the contractions, or it may be caused mechanically by the arrangement of the 
 apparatus. Thus, when the clamp is not very tight the movements of both auricle and ventricle are 
 transmitted mechanically through the clamp to the other side, so that the contraction of the ventricle not 
 only pulls the lower lever upwards but also slightly moves the upper lever downwards, and the reverse 
 with the contractions of the auricles ; therefore, if the ventricular contraction comes before the auricular 
 lever has reached its lowest position of relaxation, then the pull of the ventricle will not only prevent 
 the auricular lever falling any lower but will also increase the size of the next auricular contraction. 
 This mechanical influence of the ventricular contractions is seen in such cases as Plate 68, fig. 14, where 
 the ventricular beats have produced the appearance of strong and weak beats in the auricular curve. 
 It is possible then to explain the rise in the diastolic line, both of auricles and ventricle, which 
 often occurs after stimulation of the vagus nerve by the fact that owing to the increase in the force of 
 the contractions, a stronger mechanical effect is produced upon the contractions of that part of the heart 
 
 * Op. cit., p. 469. 
 
1022 DR, W. H. GASKELL ON THE RHrTHM OF THE HEART OF 
 
 which is situated on the opposite side of the clamp. That this will help to explain many of the cases of 
 diminished relaxation after vagus stimulation there can be no doubt. Still, I have seen cases in which 
 such an explanation does not seem sufficient, especially when the ventricle is beating with alternately 
 strong and weak beats. 
 
 Further, such an explanation will not account for the peculiar shape of the diastolic line in the series 
 of ventricular beats which occur as a consequence of vagus stimulation when the ventricle has been 
 reduced to standstill either by tightening the clamp or heating the auricles and sinus. The series of 
 curves given in Plate 69, figs. 17 and 18, show, firstly, that when the ventricle is made to beat with the 
 same rhythm as the auricles the relaxation between the beats is very much less than that of the quiescent 
 ventricle ; and, secondly, that the muscle relaxes less between consecutive beats near the commencement of 
 each group of beats than later on in that group, although as is seen in curve C, fig. 17, the rate of rhythm 
 has remained the same throughout the series of beats. This diminution of relaxation at the commence- 
 ment of each group is clearly not due to any mechanical action of the auricular contractions ; for, as is 
 seen in all the figures, and especially in fig. 18, where the maximum contractions of the auricles occurred 
 before the ventricle began to beat, those contractions caused no appreciable efiect upon the position of 
 the ventricular lever. 
 
 I am inclined, therefore, to think that it is possible that the increase of the contraction force caused by 
 the action of the vagus nerve may be accompanied by an increase of tonicity, and that the diminution m 
 the contraction force is certainly accompanied by a diminution of tonicity. I am the more emboldened to 
 consider this a possibility by the fact that Aubert* has already, from observations on the action of the 
 Dog's heart, suggested that cardio-tonic nerves for the heart exist, and by their action cause the greater 
 relaxation which exists during the stimulation of the vagus and the diminution of relaxation which he 
 noticed after the end of the stimulation of the nerve. 
 
 The effect of atropin, muscarin, and curare upon the action of the vagus. 
 
 Before mentioning the effect of these poisons upon the vagus action, I will endeavour 
 to sum up briefly their actions upon the motor ganglia and the muscular tissue 
 respectively, as far, at least, as can be judged from these present experiments. 
 
 Atropin applied to the ventricle alone does not alter its rate of rhythm or the force 
 of its contraction except after repeated applications. From this we can say that 
 atropin does not prevent the muscle from contracting to its full extent or diminish its 
 excitability except in extreme doses. 
 
 Muscarin applied to the ventricle alone rapidily diminishes the force of its contrac- 
 tions without altering the rate of rhythm, and may ultimately make the ventricle beat 
 synchronously with every second auricular beat. Muscarin, therefore, prevents the 
 full contraction of the muscle and diminishes its excitabihty. 
 
 Curare applied to the ventricle alone produces at first no alteration in the force of 
 its contractions or in its rhythm ; after repeated doses it diminishes the contraction 
 force and often causes the ventricle to respond once only to every two auricle contrac- 
 tions. Curare, therefore, ultimately prevents the full contraction of the muscle and 
 lowers its excitability. 
 
 Atropin apphed to the sinus and auricles only, slows the rhythm both of auricles 
 and ventricle. With this slowing it causes the ventricle to beat synchronously with 
 
 * Plugee's Archiv, Bd. -v., S. 621. 
 
THE VROQ, AND ON THE ACTION OF TEE VAGtJS NERVE. 1023 
 
 the auricles, if it has previously been beating with half-rhythm, and increases the 
 strength of the contractions both of auricles and ventricle. Also as long as the auricles 
 are beating, the ventricle beats synchronously with them. From these facts I conclude 
 that atropin slows the rate of the discharges from the motor ganglia without making 
 them weaker ; with the slower rate the impulses are therefore stronger than before, 
 and the contractions must also be stronger, up to a certain extent of slowing, because 
 with a certain slow rate of rhythm the maximum contractions of the heart are obtained. 
 Whether the sti'ength of the impulses is absolutely increased apart from the presumably 
 beneficial effects of the slower rate I cannot say positively, though I am inclined to 
 think they m&j be, as in some cases it has seemed to me that after atropin has been 
 given it is necessary to screw the clamp up tighter than usual in order to cause the 
 ventricle to remain quiescent. 
 
 Muscarin apphed to the auricles and sinus only, slows the rhythm both of auricles 
 and ventricle, weakens the auricular contractions, and may cause the ventricle to beat 
 w^th half-rhythm or to remain quiescent, before the auricular contractions have ceased. 
 This shows that muscarin not only slows the rate of the discharges from the motor 
 ganglia but also weakens the strength of the impulses. 
 
 Curare applied to the auricles and sinus only, produces at first hardly any effect ; it 
 soon, however, slows the rhythm and may ultimately cause the ventricle to beat with 
 half-rhythm. It therefore slows the rate of discharges from the motor ganglia and 
 ultimately weakens the strength of the impulses. 
 
 If the heart be suspended with the cut-open ventricle downwards and muscarin be 
 applied to the ventricle alone, then the ventricular beats are weakened without altering 
 the rhythm, as in Plate 70, fig. 26, curve A. If the preparation be now turned over 
 without loosening the clamp, so that the aiiricles are downwards, atropin can be applied to 
 the auricles and sinus alone without any chance of its reaching the ventricle. Then, as is 
 seen in Plate 70, fig. 26, curve B, where the atropin was applied to the auricles and sinus 
 at the point denoted by the arrow, the rhythm both of aiiriclesand ventricle is slowed, 
 and in consequence the ventricular as well as the auricular contractions are slightly 
 strengthened in force. If, now, atropin be applied to the ventricle, the ventricular 
 contractions immediately increase very greatly in strength, as is shown in Plate 70, 
 fig. 26, curve C, which is the direct continuation of the curve B. This shows that 
 atropin removes the weakening effect of muscarin on the muscular tissue itself 
 
 Again, if the heart be beating slowly in consequence of the application of muscarin 
 to the sinus and auricles alone, then atropin applied to the tissue on the same side of 
 the clamp does not quicken the rate of rhythm, although it may cause the auricular 
 beats to become stronger. Atropin, however, may undoubtedly cause the heart to 
 beat again when it has ceased beating from the application of muscarin. 
 
 We are now in a position to consider the effects of these three poisons upon the action 
 of the vagus nerve, and I will take first the case of atropin upon the whole heart. 
 
 Atropin when applied to the whole heart ultimately removes all the different effects 
 
 MDCCCLXXXII. 6 P 
 
1024 DR. W. H. QASKELL OX THE RHYTHM OF THE HEART 01* 
 
 of vagus stimulation, it prevents any diminution of the force of the contractions, and 
 d, fortiori any standstill, it prevents a.ny increase of the contraction force and it 
 prevents any acceleration. Examination of the various atropin curves which I possess 
 shows that the first effect of ati'opin is to lessen the extent of the diminution of the 
 force of the contractions caused by the stimulation of the nerve, so that in this stage 
 the vagus finally produces acceleration"'' and augmentation of the beats only. In the 
 further stage with the slow vigorous contractions characteristic of the atropinized 
 heart, less and less acceleration and less and less augmentation of the force of the 
 beats occurs, until at last stimulation of the nerve, even with the strongest current, 
 is absolutely ineffective. 
 
 This experiment not only proves tiiafc atropin prevents tlie action of the vagus, but it also does away 
 with an objection that might by some possibility be made against such results of vagus stimulation as I 
 have recorded, viz. ; that they are due, in part at all events, to escape of current, an objection which I 
 believe has already been urged against Sohelske'sI assertion that in certain cases where the heart was 
 not beating, he was able to make it beat again by stimulation of the vagus. I have, however, satisfied 
 myself, apart from the action of atropin, that the effects seen are due to the vagus stimulation alone, and 
 not to any escape of current. Thus the space between the electrodes and the tissue is considerable, and 
 great care was always taken that there" should be no communication between the electrodes and the heart 
 except by means of the bare nerve. Again, if the thread to which the nerve is attached be first well 
 moistened and then placed on the electrodes instead of the nerve, no effect whatever is produced upon 
 sending the current through, although upon gently drawing the nerve on the electrodes which have 
 throughout remained in the same position, the characteristic efiect is immediately produced on stimulation. 
 Also if the electrodes be placed dii-ectly upon the tissue between the heart and the forceps which hold the 
 oesophagus, no effect whatever is produced on the heart with a current of the same strength as is sufiicient 
 to cause all the effects which are seen when the nerve is stimulated. 
 
 Since the vagus acts both upon the motor ganglion and the muscular tissue, and 
 atropin is able to remove the whole effect of the action of the nerve, it naturally 
 follows that by the local action of poisons it may be possible to abolish the vagus action 
 in one part of the heart while leaving it intact in another. With this view I have 
 applied the poisons either to the ventricle alone or to the sinus and auricles alone, and 
 have obtained certain somewhat strikmg results ; at the same time the number of 
 these experiments is hardly sufficient as yet to allow me to say that these results are 
 in every case so constant as to be entirely due to the action of the poison upon the 
 sinus and auricles in one case or the ventricle in the other. 
 
 Thus, for instance, in Plate 70, fig. 27, muscarin had been applied to the sinus and auricles only, until, 
 as is seen, the auricular beats had become slow, irregular, and somewhat weaker. The vagus was stimulated 
 between the two vertical lines, and, as the figure shows, no effect was produced either on the rhythm or 
 on the force of the auricular contractions (although previous to application of the muscarin the auricular 
 contractions were augmented in force by the nerve stimulation) ; while on the other hand the ventricular 
 contractions were increased in force to as great an extent as at the beginning of the experiment. Also the 
 
 * RcBiFF, Molesch. Unters., 1865, S. 58. 
 
 t Ueber die Veranderungen der Errogbarkeit durch d. Wiirme, S. -20. Heidelberg, 1860. 
 
THE FROG, AND ON THE ACTION OF THE VAGUS NERVE. 1025 
 
 fact tliat the ventricular rliythm was throughout the same as the auricular shows that the muscarin had 
 caused the slowness and u-regularity of the rhythm by its action upon the motor ganglia, and not because 
 it had rendered the auricular muscle unable to respond to eveiy impulse. The curve affords, too, a good 
 proof that separate and not continuous impulses pass from the ganglia to the ventricle, otherwise it is 
 impossible to conceive that with the increased excitability of the muscle caused by the vagus action it 
 would be obliged to contract in the same slow irregular manner as the auricles. 
 
 Very soon after this curve was taken the muscarin caused the action of the motor ganglia to cease 
 altogether, and then it was found that stimulation of the vagus was unable' to make either ventricle or 
 auricle beat. 
 
 Tills shows that the vagus is not a motor nerve to the muscle, for if it were so 
 it must have caused contractions of the ventricle, seeing how powerfully it had been 
 able to aflPect the ventricle a A-ery short time before. 
 
 Again, cases occur where the cuives show that muscarin applied to the auricular side only had very 
 greatly reduced the size of the auricular beats, somewhat slowed the rhythm, and by its weakening action 
 on the strength of the impulses caused the ventricle (which had previously been beating synchronously 
 with the auricles) to remain quiescent. Stimulation of the nerve produced only a slight quickening of 
 the auricular beats, and after the end of the stimulation a series of ventricular beats similar to what has 
 already been described when the ventricles were reduced to standstill either by clamping or heating the 
 auricles and sinus. 
 
 Muscarin, then, is apparently able to prevent the action of the vagus upon the 
 auricles when appHed to the auricles and sinus alone, without thereby preventing the 
 action of the nerve upon the ventricle. 
 
 When atropin is applied to the sinus and auricles alone, then, simultaneously with 
 the appearance of the slow vigorous beats thereby caused, the action of the vagus both 
 on the rate of rhythm and upon the force of the ventricular as well as the auricular 
 contractions entirely disappears. In fact, atropin applied to the sinus and auricles 
 alone is as effective as when applied to the whole heart. 
 
 Cm-are applied to the auricles and sinus alone is able to prevent the action of the 
 vagus nerve upon the auricular muscle, as far, at all events, as the diminution of the 
 force of the contractions is concerned, without, as in the case of muscarin, greatly 
 diminishing the'^force of the auricular contractions, while at the same time it leaves 
 intact the action of the nerve upon the force of the ventricular contractions. 
 
 When any one of these three poisons is applied to the ventricle alone, the action of 
 the vagus upon the force of the ventricular contractions is gradually removed without 
 affecting its action upon the rhythm of the heart or upon the force of the auricular 
 contractions. The usual sequence of events is as follows : — Soon after the application 
 of the poison the nerve stimulation is no longer able to cause any diminution of the 
 force of the contractions of the ventricle, so that in this stage it causes simply an 
 mcrease of force with acceleration, if the auricular beats are accelerated. The 
 maximum of this increase is less, and takes place later after the stimulation than 
 before the application of the poison. As the action of the poison continues, the 
 ventricular beats become smaller and smaller, and the augmentation of their con- 
 tractions due to the vagus stimulation becomes less and less marked, until at last the 
 
 6 P 2 
 
1026 DR. W. H. GASKBLL ON THE RHYTHM OF THE HEART OF 
 
 vagus produces no alteration in the size of the contractions, but only an alteration of 
 rhythm in accordance with the alteration of rate of the auricular contractions." 
 
 Conclusion. 
 
 The curves and arguments given in this paper show clearly that the vagus nerve 
 exercises a powerful influence upon the muscular tissue of the heart as well as upon 
 the motor ganglia. That it acts upon the muscular tissue is proved by the fact that 
 its stimulation causes a profound alteration of the force of the muscular contractions, 
 together with corresponding variations in the excitability and tonicity of the muscle, 
 without necessarily altering the rate of rhythm. 
 
 Its action upon the force of the contractions may be in the direction of diminution or 
 of augmentation, so that the nerve sometimes causes a diminution of the force of the 
 contractions followed by augmentation, sometimes augmentation alone without any 
 previous diminution. 
 
 This diminution may vary greatly both in extent and duration ; it may be very 
 shght or so great that the contractions disappear altogether, so that in this way complete 
 quiescence may be caused ; it may be that the first few beats only after the beginning 
 of the stimulation are affected or the effect may continue until some little time after 
 the end of the stimulation. 
 
 The extent of this diminution is in close connexion with the nutritive condition of 
 the heart, so that quiescence followed by augmentation is more likely to occur when 
 the heart is first suspended ; and augmentation alone, without previous diminution, 
 after the heart has been removed from the circulation for some time. 
 
 Augmentation, therefore, without a previous diminution, is that effect of the stimu- 
 lation of the vagus upon the muscular tissue which is the most enduring ; and in 
 accordance with this, poisons which gradually prevent the whole action of the vagus 
 upon the muscular tissue always remove first the power of the nerve to cause a dimi- 
 ntition of the force of the contractions, and d fortiori quiescence, and afterwards its 
 power to cause augmentation of that force. 
 
 The vagus, also, in all probability acts upon the motor ganglia in the same direction 
 as upon the muscular tissue. It is able at one time to cause slowing, at another 
 acceleration without a previous slowing. The slowing is more likely to occur before 
 removal of the heart, or immediately after the heart has been suspended ; acceleration 
 alone or no effect at all after the removal of the circulation or after the heart has been 
 suspended some time. 
 
 So, too, poisons which enthely remove the action of the vagus first prevent the nerve 
 from causing slowing, and only finally prevent the causation of acceleration. 
 
 If, then, we compare slowing of the rate of the discharges from the motor ganglia to 
 
 * N.B.— The hearts of Toads are apparently less susceptible to the action of all three of these poisona 
 than those of Frogs. For instance, it takes much longer time to remove the whole effect of the action of 
 the vagus by means of atropin (1 p. c. solution) in the case of the former than in the case of the latter. 
 
THE FROG, AND ON THE ACTION OF THE VAGUS NERVE. 1027 
 
 diminution of the force of the contractions of tlie cardiac muscle, and acceleration of 
 that rate to augmentation of that force, we can say that the action of the vagus upon 
 all parts of the heart is similar ; and that the difference of its action at different times 
 depends not upon a multiplicity of nerve fibres, each possessing different functions, but 
 rather upon the different effects produced by the same nerve in consequence of varia- 
 tions in the condition of nutrition of the heart as a whole — variations of nutrition 
 to which naturally the more delicately-organised ganglion cells would prove more 
 sensitive than the comparatively coarser muscular fibres. 
 
 How, then, can we imagine to ourselves the action of the nerve upon the heart ? In 
 the first place, it is clear that the nerve cannot be considered as the motor nerve of 
 the muscle in the sense in which the words motor nerve are ordinarily used. The 
 nerve itself cannot upon stimulation cause a contraction of the cardiac muscle ; but 
 causes such a modification in the chemical processes going on in the muscle as to 
 modify the force of the contractions which take place when the impulses from the 
 motor ganglia reach the muscle. In fact, two distinct processes are going on — the one, 
 motor, represented by the impulses from the motor ganglia, and corresponding to the 
 blow by which such an explosive substance as nitro-glycerine, for instance, is exploded ; 
 the other, trophic, represented by the action of the vagus upon the muscular sub- 
 stance, and corresponding to something affecting the nature or properties of the 
 explosive substance itself. 
 
 The problem, then, to be explained is, what conception can be formed of the nature 
 of the changes caused in the muscle by the action of the nerve, which shall satisfy the 
 conditions that the same nerve can produce in different cases a graduated series of 
 different effects extending from a simple increase in the force of the contractions on 
 the one side down to diminution of force even to complete standstill on the other ? 
 
 In trying to form a theory to explain new facts, it is always advisable to see if any 
 theory which has been devised to explain somewhat similar facts will apply to this case 
 also. With this consideration I cannot help thinking that the recent views which 
 have been put forward to explain the changes going on in gland cells in a condition of 
 rest and activity may help in the conception of the changes going on in the cardiac 
 muscle cells under the influence of such a nerve as the vagus. In all secretory glands it 
 appears to be the fact that the formation of the ultimate products of secretion is a 
 gradual process, three stages of which can be recognised, viz. : the growth of the proto- 
 plasm, the formation of zymogen from the protoplasm, and the formation of the ultimate 
 products from the zymogen ; and according to Langlev"'' these three processes not only 
 go on at the same time, but also there may be, under different circumstances, a dif- 
 ference in the relative rates at which they proceed. 
 
 If, then, we imagine in the cardiac muscle an initial or ground substance, or, in corre- 
 spondence with the gland cell, a muscle protoplasm and a final or explosive substance 
 which is not self-explosible, but requires a stimulus to fire it ofi^. then we may conceive 
 
 * PMl. Trans., Part III., 1881. 
 
1028 DB.. W. H. GASKELL ON THE RHYTHM OF THE HEART OF 
 
 that the protoplasm does not form the explosive substance directly, but that there are 
 intermediate stages corresponding to the zymogenic stage in the gland. According to 
 this view there would be in the cardiac muscle during its normal activity three pro- 
 cesses going on : the growth of the protoplasm with the aid of the raw material from 
 the nutritive fluid surrounding the muscle fibres ; the transformation of the protoplasm 
 into intermediate products, which are non-explosible, or at least explosible with diffi- 
 culty ; and the formation from these of easily explosible material ; in fact, a gradual 
 succession from stable to more and more unstable combinations. If, then, the formative 
 activity of the muscle be distributed over these three stages in the right proportion, it 
 follows that impulses passing to the muscle at equal times must all cause contractions 
 of equal force. If, however, that activity be exclusively directed towards the forma- 
 tion of the muscle protoplasm or the intermediate non-explosible substances it is con- 
 ceivable that no contractions should be able to take place, because no suitable material 
 was ready for the impulses to act upon, though as a natural consequence of this greater 
 activity in the formation of the intermediate substances the ultimate effect would be 
 that the subsequent contractions would be very much greater than before. On this 
 view, then, the force of the contraction at any time depends upon the relative rates 
 at which these three processes proceed. 
 
 In this way I can imagine standstill to take place, and it is also quite conceivable 
 that in certain conditions of nutrition of the heart it may occur more easily than in 
 others ; thus, as we have seen in the heart cut out and suspended, complete quiescence 
 may in some cases be easily obtained, in others not at aU ; so, also, in the heart through 
 which salt solution is flowing I have often obtained standstill upon stimulation of the 
 vagus, thus confirming Ludwig and Ltjchsinger,* while in other cases I have only 
 obtained acceleration, thus confirming ScHiFF.t 
 
 Again, if the whole heart or the ventricle alone be beating in the apparatus described 
 on page 1019, while salt solution is flowing through it, it will beat regularly and well 
 for a long time with the salt solution, and if while it is still beating, whether strongly 
 or weakly, blood solution be sent into it under the same conditions of pressure, &c., as 
 the salt solution, then it often happens that as soon as the blood is seen to reach the 
 heart or the ventricle the heart stops still in the relaxed condition, sometimes for a 
 considei-able length of time, and subsequently begins again to beat with the improved 
 beats due to the blood solution. In the same heart this experiment may be repeated 
 again and again ; in other hearts the sudden supply of nutrient material contained in 
 the blood does not cause any stoppage whatever, but a simple gradual improvement in 
 the contractions. Upon the hypothesis suggested above this means that in consequence 
 of the sudden supply of blood the whole energy available is in the one case engao-ed 
 in the growth of the protoplasm from the raw material, so that no contractions can 
 take place, while in the other it is distributed more equally over the different processes 
 going on in the muscle. 
 
 * Op. cit. -j- Op. cit. 
 
THE FROG, AND ON THE ACTION OE THE VAGUS NERVE. 1029 
 
 As a conceivable hypothesis, then, it seems to me we may say — the vagtis increases 
 the activity of the formative processes going on in the muscle, and it will produce 
 therefore augmentation of the force of the contractions alone, or diminution followed 
 by augmentation, or even standstill followed by augmentation, according as that 
 activity is more or less equally distributed over the different stages of the process, the 
 ultimate end of which is the forma,tion of the final contractile substance. 
 
 Again, although I am not prepared at present to offer any definite theory to explain 
 the action of the nerve upon the motor ganglia, yet still it is impossible to help being 
 struck with the apparent resemblances between its action on these cells and on the 
 muscle cells ; thus just as in the case of the muscle the nerve may at one time cause 
 diminution followed by augmentation of the contractions, at another time augmenta- 
 tion alone "without any previous diminution, so in the case of the motor nerve cells, 
 the vagus may under certain conditions cause a slowing of the rate of discharge of the 
 impulses followed by acceleration, under other conditions acceleration alone without 
 any previous slowing. 
 
 I ventvu'e, therefore, to suggest that — 
 
 The vagus is the trophic nerve of both the muscular tissue and the motor ganglia, 
 meaning thereby that it increases the activity of the various formative pro- 
 cesses going on in both these kinds of tissue, and it produces all its effects 
 by virtue of this quality. 
 
 In all that I have hitherto said I have been speakmg entirely of the hearts of Frogs 
 and Toads, and so far as these animals are concerned I venture to think that my views 
 are in harmony with an experiment of Foster and Dew-Smith,* who showed that 
 although the constant current was able to cause rhythmical contractions in the isolated 
 and quiescent apex or ventricle, or in the whole heart when rendered quiescent by the 
 Stannius ligature, yet it was unable to do so when the heart was reduced to standstill 
 by the stimulation of the vagus. This remarkable experiment, which, as far as I know, 
 has never been disputed or explained, seems to me to follow naturally from the experi- 
 ments and conclusions put forward in this paper. 
 
 As yet I have not made any experiments upon the hearts of warm-blooded animals, 
 and cannot therefore assert from my own observations that the vagus acts in a similar 
 way upon them ; there are, however, certain experiments recorded which render this 
 conclusion more or less probable. Thus Panum and GlANUZZit have both observed 
 that in Rabbits with weakly -beating hearts, stimulation of the vagus causes the beats 
 to become much stronger. TraubeJ has observed that in a curarised animal the heart 
 beats for a longer time after the cessation of artificial respiration with the vagi intact 
 than when these nerves have been previously cut ; and Brown-Sequaed§ has quite 
 
 * Journ. Anat. and Physiol., vol. x. 
 
 t Hermann's Handbuoh der PhyioL, Bd. iv., S. 384. 
 
 t Allgem. Med. Centralzeitiing, 1864, N. 42. 
 
 § Gaz. Med, de Paris, 1880, p. 391. 
 
1030 DR. W. H. GASKELL ON THE RHYTHM OF THE HEART OF 
 
 recently noticed that if two Rabbits are killed at the same moment by cutting open 
 the aorta, and if in the one the vagus has been strongly stimulated just before the 
 aorta is opened and not in the other, then that heart which has been affected by the 
 nerve stimulation will beat stronger and continue to beat a longer time than the heart 
 of the Rabbit in which the vagus had not been stimulated. 
 
 These experiments render it probable that the action of the vagus on the warm- 
 blooded is similar to its action on the cold-blooded heart. 
 
 Evidence of another kind is given by the observations of Eichorst* and ZANDEB,,t 
 who find that the death which results from section of both vagi is not entirely due to 
 inanition, but partly to degenerative changes in the heart itself; they therefore con- 
 clude that the vagi nerves exercise a trophic influence on the heart. 
 
 Hitherto I have tacitly assumed that the vagus acts directly upon the muscular 
 tissue a,nd the motor ganglia respectively, and not through the aid of some intermediate 
 apparatus. Now although the experiments with muscarin and curare which I have 
 just mentioned tend to confirm this view, for in each case the local application produced 
 only local results whether upon the muscle or on the motor ganglia, yet the action of 
 atropin is difficult to explain on this hypothesis. If atropin acts directly upon the 
 muscular tissue and the motor ganglia, so as in each case to slow the rate at which 
 the formative processes are going on, without at the same time diminishing the extent 
 of those processes, then it is possible to conceive it as acting in direct opposition to 
 such an influence as the vagus nerve which I have supposed to act by expediting those 
 same formative processes ; were this the whole of its action, however, it ought to prove 
 as local in its effects as muscarin or curare. Since, however, atropin removes the whole 
 action of the vagus nerve upon the ventricle when it has been applied to the sinus and 
 auricles only, the question naturally arises, how is this to be explained ? Is there a 
 trophic centre for the ventricle which is situated either in the auricles or venous sinus, 
 upon which both atropin and the vagus act ? At present I do not see any absolute 
 necessity to draw such a conclusion from this action of atropin, and therefore prefer to 
 leave this question entirely undecided in the hope that further researches may enable 
 me to come to some deflnite conclusion upon the matter. 
 
 In conclusion, I desire again to call attention to the fact that the action of the vagus 
 upon tlie muscular tissue of the heart is characterised by two different sets of effects. 
 
 1. Diminution of contraction force associated with a diminution in the excitability 
 and a diminution of the tonicity of the cardiac muscle. 
 
 2. Increase of contraction force associated with an increase in the excitability and 
 possibly also with an increase in the tonicity of the cardiac muscle. 
 
 Upon the view put forth above that a series of substances are formed between the 
 muscle protoplasm and the final explosive substance, it follows that the chemical 
 combinations which are formed in the lower part of this series possess less explosive 
 
 * ' Die trophisclien Bezichtmgen der Nervi Vagi zum Herzmuskel.' Berlin, 1878. 
 t Pflugee's Archiv, Bd. xix., S. 263. 
 
THE FROG, AND ON THE ACTION OF THE VAGUS NERVE. 1031 
 
 energy, are less excitable, and less compact than the combinations which occiir in the 
 higher part of the series. Finally, I cannot help being struck with the fact that 
 alkaline substances such as sodium hydrate or sodium carbonate increase the excita- 
 bility, increase the tonicity and increase the force of the contractions in weakly-beating 
 hearts ; while, on the other hand, such substances as lactic acid diminish the excitability, 
 diminish the tonicity and diminish the force of the contractions of the cardiac muscle. 
 Whether the resemblance in these two cases is purely fictitious, or whether the trophic 
 action of the vagus nerve is connected with some such action of acids and alkalies I 
 cannot say, and only put forward the resemblance in the hope that a possible clue 
 may thus be found to the chemical action of the vagus upon the muscular substance of 
 the heart. 
 
 Postscript. 
 
 (Added July 3rd, 1882.) 
 
 Throughout this paper I have spoken of impulses proceeding from the sinus to the 
 ventricle without attempting to define the nature of the stimulus which causes the 
 ventricle to contract, or the path along which the impulse travels. Subsequent 
 investigations which I have made upon the hearts of Tortoises have thrown new light 
 vipon the cause of the sequence of the ventricular upon the auricular beat, and point 
 to a possible explanation of the want of sequence observed under different circumstances 
 which is somewhat different to that suggested above. 
 
 The heart of the Tortoise is removed from the body and suspended between two 
 levers in the manner above described ; no clamp is used, but the aortic trunk is held 
 firmly in a suitable holder. By means of section of the auricle in difierent directions 
 and to different extents I find that — 
 
 1. The sequence of the ventricular upon the auricular contractions is associated with 
 the passage of a wave of contraction along the auricular muscular fibres to the auriculo- 
 ventricular groove, and is not dependent upon the integrity of the large nerve trunks 
 between the sinus and the ventricle. 
 
 2. By means of section of the auricle the passage of this wave can be blocked and 
 the ventricle in consequence remains quiescent. 
 
 3. If the section be severe the block will be complete ; no contractions will pass. If 
 less severe, the block will be partial and then every second contraction will pass, and as 
 soon as it reaches the auriculo-ventricular groove will cause a contraction of the 
 ventricle. 
 
 In this way by hindering the passage of a contraction wave to the ventricle, the 
 ventricle can be made to beat with every second contraction of the sinus and that 
 part of the auricle in connexion with the sinus, in precisely the same way as by 
 tightening the clamp between the sinus and ventricle of the Frog. The probability 
 therefore is strong that the clamp produces the half-rhythm observed because it blocks 
 
 MDCCCLXXXII. G Q 
 
1032 BR. W. H. GASKELL ON THE RHYTHM OF THE HEART OE 
 
 the passage of a contraction wave to the ventricle, and not because it w^eakens a 
 nervous impulse from the sinus to the ventricle. 
 
 Again, when by section of the auricle of the Tortoise only every second contraction 
 passes the block and induces a contraction of the ventricle, stimulation of the vagus 
 is able to cause every contraction to pass, in a manner similar to that observed in the 
 case of the Frog when the clamp was tightened. This, then, would seem to show that 
 in this latter case too the vagus produced this effect, not so much by its influence upon 
 the excitability of the ventricular muscle as by its power to remove the blocking of 
 the auncular contractions caused by the pressure of the clamp upon the auricular 
 fibres at their termination in the auriculo-ventricular groove. 
 
 Lastly, I find that with a section of the auricular muscle, such that every contrac- 
 tion is able to pass at a certain rhythm, only every second contraction passes at a 
 quicker rhythm ; i.e., the time required for the auricular tissue to recover itself after 
 a contraction is much longer at the blocking point than at other parts of the auricle. 
 In this way many cases of half-rhythm which are coincident with an increased rapidity 
 of rhythm are to be explained. 
 
 Description of Figures. 
 
 In all the figures the divisions on the line ti'aced by the time marker correspond to 
 intervals of two seconds. The duration of the vagus stimulation is in all cases marked 
 by two thin vertical lines. All the curves read from left to right. 
 
 PLATES 66-70. 
 
 Fig. 1. March 17; 1881. Frog. Auricles and sinus alone heated between the two 
 
 vertical lines. 
 Fig. 2. March 28, 1881. Toad. Ventricle alone heated between the two vertical 
 
 lines. 
 Fig. 3. June 17, 1881. Frog. Clamp in auriculo-ventricular groove tightened at the 
 
 place denoted by the arrow. 
 Fig. 4. Feb. 16, 1881. Frog. Stimulation of vagus. Sec. coil at 13 centims. No 
 
 clamp. Ventricular beats only registered. 
 Fig. 5. March 17, 1881. Frog. Stimulation of vagus. Sec. coil at 10 centims. 
 
 Auricles and sinus were heated. In consequence, auricles are beating very 
 
 rapidly, and ventricle does not respond to every auricular beat. 
 Fig. 6. March 15, 1881. Frog. Stimulation of vagus. Sec. coil at 8 centims. The 
 
 stimulation was probably weaker for some reason in curve A than in curve B. 
 Fig. 7. March 8, 1881. Frog. Stimulation of vagus. Sec. coil at 10 centims. The 
 
 auricular contractions are just visible during the ventricular standstill. 
 Fig. 8. June 23, 1881. Toad. Stimulation of vagus. Sec. coil at 10 centims. 
 
THE FROG, AND ON THE ACTION OF THE VAGUS NERVE. 1033 
 
 Fig. 9. June 20, 1881. Toad. Stimulation of vagus. Sec. coil at 10 centims. 
 
 Fig. 10. April 11, 1881. Toad. Stimulation of vagus. Sec. coil at 5 centims. The 
 ventricle was unable to register the maximum of its contractions, as the 
 upper and lower levers came in contact. 
 
 Fig. 11. March 1, 1881. Frog. Curve B. Stimulation of vagus. Sec. coil gradually 
 pushed from 15 to 8 centims. 
 
 Fig. 12. March 1.5, 1881. Frog. Stimulation of vagus. Sec. coil at 5 centims. 
 Auricular beats only shown. Curve B is the continuation of curve A, except 
 that the vagus was stimulated between the two curves. 
 
 Fig. 13. March 10, 1881. Frog. Stimulation of the vagus. Sec. coil at 10 centims. 
 
 Fig. 14. May 12, 1881. Toad. Stimulation of vagus. Sec. coil at 8 centims. Ven- 
 tricle beating once to every 3 auricular beats. 
 
 Fig. 15. April 11, 1881. Toad. Stimulation of vagus. Sec. coil at 10 centims. 
 
 Fig. 16. Feb. 25, 1881. Frog. Stimulation of vagus. Sec. coil at 8 centims. Con- 
 tractions of base of ventricle, upper curve ; of apex, lower curve. 
 March 17, 1881. Frog. Curves A, B, C, D. Series of curves to show effect 
 of vagus stimulation, when the ventricle is rendered quiescent, by heating 
 the auricles and sinus. 
 
 June 6, 1881. Toad. Stimulation of vagus. Sec. coil at 7 centims. Clamp 
 tightened so as to render ventricle quiescent. 
 
 May 9, 1881. Frog. Stimulation of vagus. Sec. coil at 9 and 8 centims. 
 Ventricle beating with alternately strong and weak contractions. Inter- 
 mediate part of the curves indicated by the dotted lines. 
 
 Feb. 23, 1881. Apex and base of ventricle. Apex beating with alternately 
 weak and strong contractions. Base upper, apex lower curve. 
 June 16, 1881. Frog. Secondary rhythm in the alternately strong and weak 
 contractions of the 'ventricle. 
 
 Figs. 22 and 23. Apparatus as described on page 1019. 
 
 Fig. 24. Nov. 4, 1880. Toad. Stimulation of the vagus. Sec. coil at 6 centims. 
 Heart in modified Boy's tonometer. Pressure of blood solution 5 centims. 
 
 Fig. 25 A and B. Nov. 4, 1880. Stimulation of vagus. Sec. coil at 4 and 3 centims. 
 Pressure of blood solution 28 centims. in A, 29 centims. in B. 
 
 Fig. 26. May 19, 1881. Frog. Curve A. Muscarin sulphate, 5 per cent, solution 
 applied to the ventricle at the point marked by an arrow. Upper curve 
 auricle, lower curve ventricle. Curve B. Atropin sulphate, 1 per cent, 
 solution applied at arrow to the auricles and sinus only. Upper curve 
 ventricle, lower curve auricle. Curve C. Atropin sulphate applied to 
 ventricle at the arrow. Upper curve ventricle, lower curve auricle. 
 
 Fio-. 27. July 16, 1881. Toad. Stimulation of vagus. Sec. coil at 10 centims. 
 Muscarin sulphate, 5 per cent, solution had been applied to the auricles and 
 
 sinus only. 
 
 6 Q 2 
 
 Fig. 
 
 17. 
 
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 18. 
 
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 19, 
 
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 20. 
 
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