236 PSYCHOLOGICAL EFFECTS OF ALCOHOL. 



to show some depression of accelerator tone, but in nothing like the 

 proportion that should theoretically obtain in a pure accelerator 

 depression. It is noteworthy that the normal of the day on the alcohol 

 day shows a rapid pulse. Even at 6 h 30 m p. m. the duration of systole 

 is slightly less than on the normal day. The failure of the pulse on the 

 alcohol day to reach the retardation of the normal day was consequently 

 due solely to a less rapid lengthening of diastole. In other words, after 

 alcohol the normal inhibitor tone was less completely or less rapidly 

 established. Whatever evidence this illustrative case may give seems 

 to indicate that the relative acceleration effected by alcohol is due to a 

 lessened responsiveness of the cardio-inhibitory mechanism. The 

 argument, however, is not entirely clear, since we are dealing with two 

 variables in the relative acceleration: (1) the alcohol change, and 

 (2) the normal relaxation change. In view of the consequent ambi- 

 guity of interpretation, we hesitated to have all the pulse-records re-read 

 to find the relative change in the duration of systole and diastole. It 

 is possible that this ought to be done, but we believe that other and 

 less ambiguous data will be more convincing. 



Even in the association-pulse there were some indications that the 

 effect of alcohol was a partial paralysis of the cardio-inhibitory mech- 

 anism. First, it will be remembered that there was little or no positive 

 acceleration of the pulse after alcohol. Our "relative acceleration" is 

 really a failure of the pulse to develop its normal retardation. That 

 seems less like the effect of positive stimulation than it does like a partial 

 paralysis of the depressor. Secondly, we noted that alcohol flattened 

 out the response of the pulse to the association process. It will be 

 remembered that the association rhythm was completely changed after 

 dose B, in Subject VII (see fig. 31). Now, it seems to be well estab- 

 lished that rapid adjustments of the pulse-rate to varying demands of 

 work and rest are effected by the inhibitor (Hunt, 1 Aulo 2 ). The accel- 

 erator reacts more slowly, with a latency of the order of 10", when it 

 reacts at all. Since the entire association cycle occupied only 10", the 

 post-stimulation change in the association pulse can not be a phenome- 

 non of the slow-acting accelerator, but must on the contrary be con- 

 ditioned bv the cardio-inhibitor mechanism. The elimination of the 



*/ 



post-stimulation pulse-change after alcohol must consequently be due 

 to a decreased responsiveness of the cardio-inhibitor mechanism. 



It was these considerations of the different latencies of the accelerator 

 and depressor mechanisms that gave special significance to a phenome- 

 non that was incidentally observed during the re-reading of the records 

 for the relative length of systole and diastole. It was observed that on 

 the normal day of Subject III, the mean variation of the diastolic pulse- 

 phases was approximately 10 per cent of the total length of diastole. 



'Hunt, Am. Journ. Physiol., 1899, 2, p. 395. 



2 Aulo, Skand. Archiv f. Physiol.. 1911, 25, p. 347. 



