318 INHIBITION AND AUGMENTATION. [BOOK i. 



in the same way as when the augmentor fibres are directly stimu- 

 lated ; there is a marked increase in the force of the auricular and 

 of the ventricular systole, and at times an obvious acceleration of 

 the rhythm. We may infer that in such a case the augmentor 

 fibres are thrown into activity through the afferent impulses as 

 part of a reflex act. At the same time it must be remembered, 

 that afferent impulses may increase the beat of the heart not by 

 exciting the augmentor mechanism, but by depressing, that is 

 by inhibiting a previously existing activity of the cardio-inhibitory 

 centre ; to this point we shall again have to refer. 



We may however conclude that both the inhibitory and the 

 augmentor mechanisms of the heart can be brought into action by 

 means of the central nervous system. Speaking broadly the effect 

 of the former is to diminish the work of the heart, and so to lower 

 the blood pressure, and that of the latter to increase the work of 

 the heart, and so to heighten the blood pressure. 



161. The question, What is the exact nature of the change 

 brought about by the inhibitory and augmenting impulses respect- 

 ively on their arrival at the heart ? or, in other words, By virtue 

 of what events produced in the heart itself do the impulses along 

 the one set of fibres bring about inhibition, along the other set 

 augmentation ? is a very difficult one, which we cannot attempt to 

 discuss fully here. 



We may of course suppose that the very impulses themselves 

 as started at the point of stimulation are, owing to the very nature 

 of the fibres, different in the one set and in the other. Many 

 phenomena however of the nervous system lead us, by analogy, to 

 the conclusion that this is not the case, but that stimulation of the 

 fibres produces different effects on the heart by reason of the 

 different ways in which the fibres end in the heart. We may for 

 instance suppose that there exist in the heart what we may call 

 an inhibitory and an augmenting mechanism with which the 

 inhibitory and augmentor fibres are respectively connected. And 

 a special action of atropin on the heart lends support to this view. 



If, either in a frog or a mammal, or other animal, after the 

 vagus fibres have been proved, by trial, to produce, upon stimu- 

 lation, the usual inhibitory effects, a small quantity of atropin 

 be introduced into the circulation (when the experiment is con- 

 ducted on a living animal, or be applied in a weak solution to 

 the heart itself when the experiment is conducted, in the 

 frog for instance, on an excised heart or after the circulation has 

 ceased), it will after a short time be found, not only that the stimu- 

 lation, the application of a current for instance, which previously 

 when applied to the vagus produced marked inhibition, now 

 produces no inhibition, but even that the strongest stimulus, the 

 strongest current applied to the vagus, will wholly fail to affect 

 the heart, provided that there be no escape of current on to the 

 cardiac tissues themselves ; under the influence of even a small 



