THE ACTION OF THE VAGUS NERVE ON THE MAMMALIAN HEART

1. The rate‐changes induced in the heart by vagus stimulation may be mediated by (a) a gradually manifested controlling influence on the normal pacemaker, or (b) a sudden displacement of the pacemaker to lower levels. 2. There may be marked divergence in the rates of auricle and ventricle apart from those depending on A‐V blocking. The auricle may be disproportionately slowed or temporarily stopped while the ventricle continues beating at a slowed rate. Under vagus influence alternation in the lead from the S‐A node and the A‐V node may occur for a time. Retrograde conduction may sometimes be associated with premature beats of auricle and ventricle. 3. Direct excitability can be depressed by the vagus and by acetylcholine in both auricle and ventricle. There is some evidence of a subsequent hyperexcitable phase in certain cases. 4. The weakening effects of the vagus, shown by tracings of auricle and ventricle, are not explicable by physical changes accompanying the slowing of rhythm, but connote a definite reduction in the contraction‐force of the auricular and ventricular muscle. This is seen not only with the circulation intact, but in the heart with its chambers empty after closure of the venœ cavœ , or in the perfused heart. 5. While many features of inhibitory weakening are similar in auricle and ventricle, there are differences in regard to the relations between the rate of rhythm and the size of the individual beats in auricle and ventricle; e.g. contractile activity excited by a series of induction shocks opposes the force‐depressing influence of the vagus or of pilocarpine in the ventricle, but not in the auricle. A similar effect, though less extensive, was found in the frog's ventricle by Fiddes. 6. The weakening power of the vagus is manifest in the ventricles in both the types of behaviour (I. and II.) described in former papers although some relations of rate‐change to force of beat are very different in the two types. The relative size of individual beat at varying intervals is determined by the interaction of two factors which are described. In type II. slowing of rhythm may often be sufficient per se to cause definite weakening. 7. Apart from vagus stimulation, the perfused heart presents resemblances, as regards the relations of rate and force, to the ventricle with intact circulation in type I. under vagus influence. 8. The vagus can cause a marked increase in the duration of the ventricular curves, affecting both contraction and relaxation phases and occurring in beats of slowed rhythm, whether such beats are large or weakened ones. The change is to be seen in both types during vagus stimulation, and in the empty ventricle as well as with intact circulation; but the auricular curves are not similarly lengthened. 9. Auricular fibrillation not infrequently occurs as an after‐effect of vagus stimulation or acetyl‐choline. 10. Vagus efficiency is often notably enhanced after adrenaline stimulation and after the administration of hirudin. 11. Some relations of the local inhibitory area in the heart are described. 12. Removal of vagus control by section or freezing commonly leads, in addition to the usual acceleration, to augmentation of the auricle and sometimes also of the ventricle, the latter being in some instances the more extensive. Ventricular augmentation is not confined to type II. where a change in rate might per se lead to increased force of beat. There may also be development of chloroform irregularity or removal of fibrillation which had been present in the auricle; in the latter case vagus section may cause slowing of the ventricular rate, instead of the usual acceleration. 13. Differences in the effects of stimulation and of section of the right and the left vagus, which have sometimes been seen, are recorded. 14. Both with the circulation intact and in the perfused heart, results have sometimes been obtained that are at first sight suggestive of a reversal of vagus action, but most, if not all, of these are explicable on other grounds. I beg to express my cordial thanks to Professor G. Spencer Melvin who was associated with me in a number of the earlier experiments of this investigation. A grant from the Medical Research Council has defrayed part of the expenses of the inquiry.