316 



THE NERVOUS REGULATION OF THE HEART 



the inhibitor mechanism. In addition, these reactions are believed 

 to be brought about with the aid of four different sets of nerve fibers. 

 In the light of the preceding discussion, however, it would seem that 

 these different peculiarities of the heart beat should rather be ascribed 

 to certain differences in the manner of distribution of these impulses 

 to the cardiac musculature. 



Another question to be considered at this time, pertains to the 

 specificity of the vagus nerve. It has been stated above that the cardio- 

 inhibitor effect can only be induced with the help of this particular 

 nerve, because it forms the sole connection between the central 

 nervous system and the inhibitor end-organs in the heart. It is, 

 however, a well-known physiological fact that the 

 character of a reaction does not depend upon the 

 nerve as such, but upon the structural and func- 

 tional peculiarities of the end-organ with which 

 it is connected. The vagus nerve does not form an 

 exception to this rule, and hence, it must be con- 

 cluded that its function is to conduct impulses, 

 II i /^ I while the inhibition depends upon certain pecu- 

 W/) 'T' AA^ liarities of the cardiac effectors. For this reason, 

 the cause of the inhibition of the heart must be 

 sought at the periphery, namely, in certain physico- 

 chemical alterations in the vagal terminals and 

 neighboring muscle cells. The specificity of the 

 vagus, therefore, is, so to speak, "accidental." 

 In substantiation of this statement, it might be 

 TO ILLUSTRATE THE mentioned that it is possible to establish a func- 

 ACTION OF NICOTIN. tional union between the central end of the divided 

 V, vagus, pregang- fifth cervical nerve and the distal stump of the 



Peculiarly enough, the excitation of. this 



and 

 cell. 



lionic path; SAP, va p;us 

 sino-auricular plexus; * 



p, postganglionic formerly musculo-motor nerve invariably leads to 

 path; 'N, nicotin an inhibition of the heart. In a similar way, this 



organ could be inhibited with the help of any other 

 postganglionic efferent nerve, but only in case a crossing of its 



fibers with those of the vagus is an experimental 



possibility. 



The preceding statements regarding the specificity of the vagus 

 find substantiation in the changes which the inhibitor reaction suffers 

 in consequence of the administration of certain drugs, such as nicotin, 

 atropin and muscarin. To illustrate, if the heart of a frog or turtle 

 is moistened with a weak solution of nicotin, the stimulation of the 

 vagus (V) becomes ineffective as soon as this agent has had sufficient 

 time to penetrate the cardiac tissues. At this time, however, the 

 excitation of the plexus at the sino-auricular junction (SAP) of the 

 heart still gives rise to an inhibition. Nicotin is a cell poison; its 

 action being centered upon the dendritic filaments of the neurone. 

 It may be concluded, therefore, that it breaks the connection between 



