RHYTHMIC ARTERIAL EXPANSION AS A FACTOR IN THE CONTROL OF HEART RATE

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Abstract
Two sets of expts. with entirely different aims are reported: 1. In a first series the heart rate changes which occur reflexly or directly when pulse pressure and mean pressure were varied as independently as possible were studied. Aortic pressures were optically recorded and systolic, diastolic and pulse pressures calculated from records by use of a calibration scale. Mean pressure values were arrived at accurately by measuring the area beneath the pressure curve and dividing by horizontal distance. The effects produced by various procedures such as compressing the vena cava and aorta served no useful purpose in settling the problem as pulse pressure and mean pressure changed in the same direction. They were useful in determining that under such conditions a mean pressure variation of 4-5 mm. is the minimal which causes any certain change in heart rate (e.g., 5 beats in 150 per min.). After saline infusion which increases the pulse pressure, a cardiac slowing was obtained in a sufficient no. of expts. in which no change or a decrease in mean pressure took place. These results were suggestive of a separate effect of puke pressure, but in view of some apparently negative effects could not be regarded as conclusive. Through the expedient of producing experimental aortic insufficiency it was found possible to increase pulse pressure and simultaneously decrease mean pressure; further by compressing the thoracic aorta to a suitable extent, mean pressure was often restored approximately or exactly to normal, while pulse pressures increased still more. It was found that frequently the heart rate slowed despite a sharp decline of mean pressure and with one exception was always retarded when mean pressure was restored to normal levels by compression. While the control of heart, rate by pulse pressure changes was demonstrated, the results on the "whole animal" permitted no conclusions as to whether the effects were induced by direct or reflex action. A 2nd set of expts. was performed to determine whether changes of pulse pressures in a cephalic end of a perfused carotid artery can reflexly cause heart rate changes either when mean pressure remains unaltered or deviates in a reverse direction. To do this, pressure pulses were recorded simultaneously from the perfused carotid and the animal''s own artery by means of optical manometers. Perfusion of the cephalic end of a carotid artery with a constant pressure in the perfusion system was found not to produce a constant pressure within the artery itself owing to effects of collateral circulations. The magnitude of the pulsation varied inversely as the perfusion pressure used, being larger when pressures were low and small when they were high. Such dynamic effects complicate the interpretation of results of previous investigations. A sudden change in pressure appeared more potent in producing temporary alterations in heart rate than permanent levels of pressure established. Alteration of the perfusion pressures and rhythmic variations such that pulse pressure increased in the perfused vessel while mean pressure remained unaltered or was even reduced were attended by cardiac slowing unless the reduction was extreme. This demonstrates that pulse pressure variation dominates the production of reflex cardiac changes. The conclusion is reached that Marey''s law requires amendment; changes in mean pressure levels indeed control heart rate changes reflexly, but only so long as pulse pressures do not change too much in an opposite direction. When this is the case the effects of pulse pressure changes dominate the reactions.

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