ISO A MANUAL OF PHYSIOLOGY 



the augmentor path, without, however, proving of itself that 

 such a difference exists. In one experiment the heart of an 

 anthropoid ape was revived when three successive periods viz., 

 four and a half, twenty-eight and a half, and fifty-three hours 

 respectively had elapsed after the death of the animal, although 

 during the last period the heart had been twice frozen hard. The 

 vagus was shown to be still capable of causing some inhibition 

 six hours after death, and the accelerans some augmentation as 

 late as fifty-three hours after death (Hering) . 



In the discussions that have arisen over the relation of the ex- 

 trinsic to the intrinsic cardiac nervous apparatus appeal has fre- 

 quently been made to the action of certain poisons on the heart. 



Thus, after nicotine has been injected subcutaneously, or painted 

 directly on the heart of a frog, stimulation of the vago-sympathetic 

 causes no inhibition ; it may cause augmentation. But stimulation 

 of the junction of the sinus and auricle still causes inhibition, as in 

 the normal heart. 



Atropine and its allies, such as daturine, not only abolish the in- 

 hibitory effect of stimulation of the vagus trunk, but also that of 

 stimulation of the junction of sinus and auricle. 



Muscarine, a poison contained in certain mushrooms (p. 183), 

 causes diastolic arrest of the heart, which, when the circulation is 

 intact, becomes swollen and engorged with blood. This action 

 takes place in a heart already poisoned with nicotine or one of its 

 congeners, but not in a heart under the influence of atropine or its 

 allies. And a heart brought to a standstill by muscarine can be 

 made to beat again by the application of atropine, although not by 

 nicotine. 



These facts may be explained as follows : Nicotine paralyzes not 

 the very ends of the vagus, but the ganglia through which its fibres 

 pass. Stimulation of the sinus, which is practically stimulation of 

 the vagus fibres between the ganglion-cells and the muscular fibres, 

 is therefore effective, although stimulation of the nerve-trunk is not 

 (Langley). On the other hand, the atropine group paralyzes the 

 nerve-endings themselves, or interferes with the reception of the 

 inhibitory impulses by acting on a so-called receptive substance in 

 the muscle (p. 166), so that neither stimulation of the sinus nor of 

 the nerve-trunk can cause inhibition. Muscarine, on the contrary, 

 stimulates the vagus fibres between the nerve-cells and the muscle, 

 or the actual nerve-endings, or exerts an inhibitory action on the 

 muscle itself through the appropriate receptive substance, and thus 

 keeps the heart in a state of permanent inhibition, which is removed 

 when atropine cuts out the nerve-endings, or combines with the 

 receptive substance. It is quite in accordance with this that mus- 

 carine has no effect on a heart whose vagus nerves, as occasionally 

 happens, have no inhibitory power. Pilocarpine has very much 

 the same action as muscarine. 



The view that muscarine and atropine can directly affect the 

 cardiac muscle gains a certain amount of support from the facts 

 that these drugs act very much in the same way on the heart of the 

 mammalian embryo (rat, rabbit, etc.) before and after the develop- 

 ment of its intrinsic nervous system, and that the passage of an 

 interrupted current through the heart of very young embryos causes 

 distinct inhibition. But, as has already been pointed out, it is not 



