i8 



Scientific Proceedings (69). 



series of experiments on normal individuals was carried out. 

 Eighteen subjects, all under twenty-eight years of age and all 

 with apparently normal hearts, were given hypodermic injections 

 of 1 mg. of atropin. The effect of deep breathing and of ocular 

 pressure upon the cardiac mechanism was studied both before and 

 during the atropin action. Before the injection, A-V rhythm was 

 not produced in any of the subjects tested. Between eight and 

 fifteen minutes after the injection, however, A-V rhythm could 

 be produced by ocular pressure or deep respiration in the majority 

 of the subjects. After the atropin effect had reached its height 

 A-V rhythm could no longer be produced. 



Three types of A-V rhythm were observed. In the first, which 

 occurred most frequently, the P-R interval was reduced and P 

 was inverted; in the second, the P-R interval was zero; while in 

 the third there was an R-P interval. The last was observed in 

 only two subjects. These differences evidently depended upon 

 the level of the pacemaker in the junctional tissues. 



These observations may be explained on the assumption that 

 atropin releases the A-V tissues from vagus control somewhat 

 before it releases the sinus node. At this time stimulation of 

 the vagus slows the sinus rhythm without a correspondingly 

 great effect upon the inherent rhythms of the lower centers. The 

 latter therefore tend to usurp the pacemaking functions of the 

 heart. After full atropin action on the other hand, both the sinus 

 and the lower centers are released and the more rapid sinus rate 

 controls the cardiac rhythm. Before atropin vagus stimulation 

 probably slows the inherent rhythms of the lower centers as well 

 as that of the sinus so that the former do not ordinarily escape. 



