CARDIAC INHIBITION AND ACCELERATION 



317 



the terminals of the vagus and the cells of the intracardiac plexus 

 (Remak's) which innervate the peripheral inhibitor mechanism. 

 Consequently, the stimulation of the preganglionic path, constituted 

 by the vagus nerve, must remain without effect, while the excitation 

 of the postganghonic path, formed by the cells of the aforesaid ganglion 

 and their distal axons, must give rise to an inhibition. 



If atropin is applied to the heart, or is administered in a general 

 way, negative results are obtained on excitation of the vagus {V), 

 as well as on excitation of the sino-auricular plexus (SAP). By infer- 

 ence, therefore, it may be concluded that this alkaloid produces a break 

 in the conducting path peripherally to this intracardiac ganglion, so 

 that the cardio-inhibitor impulses are no longer able to reach the end- 



FiG. 167. Fig. 168. 



Fig. 167. — -Schema to Illustrate the Action of Atropin. 



V, vagus, preganglionic path; SAP, sino-auricular plexus; P, postganglionic path; 

 A, atropin breaks theconnection between thepostganglionic pathandthecardiac muscle. 



Fig. 168. — Schema to Illustrate the Action of Muscarin. 

 V, vagus, preganglionic path; SAP, sino-auricular plexus; P, postganglionic path; 

 M, muscarin breaks the connection at the neural junction or paralyzes the musculature 

 itself. 



organ. The cardio-accelerator influences, on the other hand, are not 

 blocked and hence, we observe at this time a marked increase in the 

 frequency of the heart. Atropin is a fiber poison and paralyzes the 

 postganglionic terminals. In time to come, this agent is oxidized or 

 is excreted in its original form. As its action wears off, conduction is 

 gradually restored so that the stimulations of the vagus and of the 

 intracardiac ganglion again become effective. 



Pilocarpin and muscarin, whether applied directly to the heart or 

 administered internally, diminish the frequency and amplitude of the 

 contractions and finally produce a diastolic stoppage. Two views 

 are held regarding the action of these drugs. It is beheved, on the 

 one hand, that they paralyze the cardiac muscle tissue directly, and, 

 on the other, that they increase the irritability of the nerve-tissue 

 in such a degree that the inhibitor mechanism is under constant 



