Nervous interference as a cause of inhibition was clearly pointed out by Bernard, and in the case of the heart has been discussed by Eanvier with his usual clearness.

In the grey matter of the spinal cord there is ample room for the slowing of nervous stimuli by transmission along paths of different lengths (p. 169), more especially as a small length of grey matter is equivalent to a great length of ordinary nerve-fibre (p. 162).

In the heart we might suppose there was no such provision, but, as Ranvier points out, the ganglion cells in the auricle have one of their fibres wound spirally, so as to give a great length in small space, and thus provide for retarda-tion and interference of stimuli (Figs. 116, 117). If we suppose that some of the nerve-fibres contained in the vagus trunk pass through these spiral ganglia while others pass on directly to the heart, we can understand that the different rates of transmission may lead to interference and stoppage of pulsation. Alterations in the rate of transmission along the spiral fibre may again convert interference into coincidence of waves and cause acceleration and increased action. If these spiral fibres are affected by drugs so that the rate of transmission of stimuli along them is altered, we can understand that the interference may in some cases be increased, in others diminished, and that an increase of interference may readily pass into the opposite condition, so that the irritation of the vagus no longer produces stoppage but acceleration of the heart, such as actually occurs on irritation of the vagus after its inhibitory power has been paralysed by atropine.

Hypothesis Regarding The Action Of The Vagus 160

Fig. 115. - After Gaskell. Tracing showing increased cardiac contractions from irritation of the vagus. [In this figure the upper tracing shows the ventricular and the lower the auricular contractions.]

We can understand also how curare and the large class of drugs which paralyse the motor nerves may destroy the inhibitory power of the vagus.