56 



Scientific Proceedings (63). 



adequately account for such a pulse; (2) irritation of the aorta 

 without insufficiency apparently caused a fall of diastolic without a 

 corresponding fall in systolic pressure; and (3) when peripheral 

 vessels were constricted by adrenalin during insufficiency the 

 normal contour returned. 



By producing temporary valvular lesions 1 while the aortic 

 pressure curve was being recorded by an optical manometer, the 

 following facts have been shown: — 



1. When a lesion is suddenly produced the change in pulse 

 occurs within the time interval of one heart beat, and when normal 

 valve action is restored the normal type of curve immediately 

 returns. The changes are too rapid to be attributed to a reflex 

 vasodilation. 



2. Irritation of the aorta never produces such a change. The 

 records submitted by Stewart as evidence are clearly due to changes 

 in heart rate. 



3. The arterial pressure curve shows that while the pressure 

 falls a little more rapidly in systole so that the pressure at the 

 beginning of diastole is slightly lower, the chief drop responsible 

 for the large pulse and low diastolic pressure occurs during diastole. 

 The fact that the chief drop occurs before the dicrotic notch, when 

 records are taken with the Hurthle manometer from animals or 

 with a sphygmograph from patients, can be attributed to instru- 

 mental error. 



4. These characteristic effects in the arterial pressure curves 

 persist after a large part of the peripheral circulation is elimi- 

 nated by clamping the thoracic aorta and, contrary to the observa- 

 tions of Stewart, the effect is intensified after adrenalin. 



5. Changes in the arterial pulse similar to those found in 

 animals can be obtained from an artificial circulation machine 

 when the peripheral resistance remains unaltered. 



These results indicate that the changes of pressure evidently 

 responsible for the collapsing pulse, cannot be due to a reflex 

 vasodilation but are due to a regurgitation of pressure into the 

 ventricle, whether with or without an actual backflow of blood 

 requires further investigation. 



2 Wiggers, Du Bois, Proc. of Soc. for Exp. Biology and Medicine, 1913, X, 87. 



