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 Zander,! 
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 and 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 definite conclusion upon the matter. 
In conclusion, I desire again to call attention to the fact that the action of the vagus 
upon the 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 tropliiscFen Bezichungen der Nervi Vagi zum Herzmuskel.’ Berlin, 1878. 
t Pflugee’s Archiv, Bd. xix., S. 263. 
