318 THE NERVOUS REGULATION OF THE HEART 



excitation. The second explanation, proposing that the inhibition is 

 due to a stimulation of this mechanism, has met with greater favor, 

 probably because it can be brought into closer relation with the view 

 regarding the action of atropin, which agent, in contradistinction to 

 muscarin, depresses the inhibitor mechanism by lessening the irri- 

 tability of the postganglionic fibers and their ramifications. This ex- 

 planation is made use of in accounting for the fact that the inhibition 

 established by pilocarpin or muscarin may be removed later on by the 

 administration of atropin. It must be evident, therefore, that this 

 agent possesses the power of neutralizing the action of muscarin so that 

 the normal rhythm may again be restored. In accordance with this 

 view, it is believed that the antagonistic action of the drugs just 

 mentioned depends upon the fact that the atropin causes the irri- 

 tability of the inhibitor end-organs to be gradually diminished. 



It must be acknowledged, however, that the first view, express- 

 ing the idea that muscarin and atropin affect the cardiac musculature 

 directly, is not without foundation. Thus, it has been shown that 

 these drugs give rise to the aforesaid functional changes even in the 

 hearts of mammalian embryos at a time when nervous structures 

 have not made their appearance as yet, or at least, long before the 

 nervous connections have been fully formed. Besides, it has been 

 established that muscarin does not affect the hearts of many verte- 

 brates. 1 This evidence, however, may be met with the objection 

 that the properties of the fully developed organ cannot justly be com- 

 pared with those of the embryonic organ, and secondly, that the ac- 

 tion of these alkaloids need not be the same in all animals. 



Some interesting data regarding the distribution of the cardiac 

 impulses may also be gathered from a number of phenomena which 

 have been described by Stannius. If a thread is tied rather loosely 

 around the heart of a frog or turtle at the sino-auricular junction, 

 the sinus continues to beat rhythmically, while the remaining portion 

 of the heart ceases its activity. This result is explicable upon the 

 basis that the wave of excitation is blocked at the seat of the ligature, 

 but it is also possible that the latter serves as a mechanical stimulus 

 to the inhibitor elements situated in the domain of the sino-auricular 

 groove (Remak's ganglion). Curiously enough, if a second ligature 

 is now applied to the heart at the auriculoventricular junction, all 

 three parts of the organ again contract, but their beats are no longer 

 coordinated. This phenomenon is difficult to explain unless it is as- 

 sumed that the second ligature stimulates certain accelerator elements 

 situated in the region of the auriculoventricular groove (Bidder's 

 ganglion). This favors the production of an independent rhythm 

 in the auricles and ventricle. 



The Cause of the Inhibition. It need scarcely be mentioned that 

 the activation of a tissue is always associated with the destruction of 



1 For a more detailed discussion, see Cushing's Pharmacology and Therapeutics, 

 London, 1915. 



