208 THE VASCULAR MECHANISM. 



have been proved by trial to produce upon stimulation the usual inhibitory 

 effects, a small quantity of atropine be introduced into the circulation (when 

 the experiment is conducted on a living animal, or be applied in a weak 

 solution to the heart itself when the experiment is conducted, as in the case 

 of a frog, on an excised heart, or after the circulation has ceased), it will 

 after a short time be found not only that the stimulation, the application of 

 a current, for instance, which previously when applied to the vagus pro- 

 duced 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 dose of 

 atropine, the strongest stimulation of the vagus will not produce standstill 

 or appreciable slowing or weakening of the beat. 



Now it might be supposed that the atropine produces this remarkable 

 effect by acting on some ganglionic or other mechanism intervening between 

 the vagus fibres and the cardiac muscular tissue ; but we have evidence 

 that the atropine acts either on the muscular tissue itself or on the very 

 endings of the nerves in the muscular fibres. We have said ( 140) that a 

 properly prepared strip of the ventricle of the tortoise will execute for a 

 long time spontaneous rhythmic contractions, it will go on "beating" for 

 a long time. A strip of the auricle will exhibit the same phenomena even 

 still more readily. If now, while such a strip from the auricle is satisfac- 

 torily beating, a gentle interrupted current be passed through it, it will 

 stop beating ; the current inhibits the spontaneous beats ; a very gentle 

 interrupted current must be used, otherwise the effect is obscured by the 

 more direct stimulating action of the current. If now the strip be gently 

 bathed with a weak solution of atropine no such inhibitory effect is pro- 

 duced by the interrupted current ; the beats go on regardless of the action 

 of the current. The interruption of this experiment is that in the first case 

 the interrupted current stimulated the fine termination of the inhibitory 

 fibres in the muscular strip, and that in the second case the atropine pro- 

 duced some effect either on these fine fibres, or on their connections with the 

 muscular substance or on the actual muscular substance itself, by virtue of 

 which they ceased to act. But if this be so, if the same inhibitory effects 

 are produced alike by stimulating the vagus trunk and stimulating the 

 very endings of the nerves in the muscles of the heart, if not the actual 

 muscular tissue itself, then there is no need to suppose the existence of any 

 special inhibitory mechanism placed between the fibres in the vagus branches 

 and the cardiac muscular tissue. 



The action of atropine on the heart is, so to speak, complemented by the 

 action of muscarine, the active principle of many poisonous mushrooms. If 

 a small quantity of muscarine be introduced into the circulation, or applied 

 directly to the heart, the beats become slow and feeble, and if the dose 

 be adequate the heart is brought to a complete standstill. The effect is 

 in some respects like that of powerful stimulation of the vagus, but the 

 standstill is much more complete, the effect is much more profound. Now 

 if, in a frog, the heart be brought to a standstill by a dose of muscarine. the 

 application of an adequate quantity of atropine will bring back the beats 

 to quite their normal strength. The one drug is, as far as the heart is con- 

 cerned (and, indeed, in many other respects), the antidote of the other. 

 And, as in the case of atropine, so in the case of muscarine, there is evi- 

 dence that the drug acts not on any ganglionic mechanisms, but on the car- 

 diac tissue itself. 



The conclusion that inhibition is the result of changes in the cardiac tis- 

 sue itself may serve to explain why in inhibition sometimes the slowing, 



