166 THE CIRCULATION OF THE BLOOD AND LYMPH 



reach the heart. The fact that the action of the accelerantes can 

 be restored by perfusing the heart with a nutrient solution at a 

 much longer interval after somatic death than the action of the 

 vagus strengthens the suggestion that ganglion-cells are interposed 

 on the inhibitory though not on the augmentor path, without, 

 however, proving of itself that such a difference exists In one 

 experiment the heart of an anthropoid ape was revived wnen thiee 

 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 over the relation of the extrinsic to the intrinsic 

 cardiac nervous apparatus appeal has frequently been made to the 

 action of certain poisons on the heart. Thus, after nicotine stimulation 

 of the vago-sympathetic causes no inhibition of the frog's heart ; it may 

 cause augmentation. But stimulation of the junction of the sinus and 

 auricle still causes inhibition. Atropine not only abolishes the inhibi- 

 tory effect of stimulation of the vagus trunk, but also that of stimula- 

 tion of the junction of sinus and auricle. Muscarine causes diastolic 

 arrest in a heart already poisoned with nicotine, but not in a heart 

 under the influence of atropine. 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. 182), 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 -end ings, 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 muscarine 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. 



Stannius' Experiment. Another series of phenomena, intimately 

 related to our present subject, have excited, since they were first made 

 known by Stannius, an enormous amount of discussion. The chief 

 facts of this classical experiment we have already mentioned (p. 144), 

 and they are also described in the Practical Exercises (p. 194). They 

 are easy to verify, but difficult to interpret. The most probable explana- 

 tion of the standstill caused by the first ligature is that the lower portion 



