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The effect of coronary perfusion pressure and preload on left ventricular systolic wall stress parameters.

作者信息

Kissling G, Dierberger B

机构信息

Physiologisches Institut II, Universität Tübingen, FRG.

出版信息

Basic Res Cardiol. 1991 Sep-Oct;86(5):476-84. doi: 10.1007/BF02190715.

DOI:10.1007/BF02190715
PMID:1768246
Abstract

The effect of coronary perfusion pressure (i.e., mean aortic pressure) and of left-ventricular preload (i.e., left-ventricular enddiastolic wall stress) on left-ventricular peak developed wall stress (sigma max) and the maximum rate of stress development (d sigma/dtmax syst) and relaxation (d sigma/dtmax diast) was examined in anesthetized rats under open-chest conditions. Pulmonary flow, aortic pressure, and left-ventricular pressure amplitude, as well as enddiastolic pressure and dP/dt were measured and the respective wall stress parameters were calculated from the measured pressure and volume data, assuming a thick-walled sphere. Aortic pressure and right-ventricular filling pressure could be adjusted independently of each other via two header tanks. A primary increase in coronary perfusion pressure results in a linear rise in sigma max, d sigma/dtmax syst, and d sigma/dtmax diast. With increasing preload, however, the systolic wall stress parameters only increase initially, run through a maximum and then decrease with further elevation of the leftventricular enddiastolic wall stress. These results are interpreted such that, at a given mean aortic pressure the wall stress developed in the left ventricle rises with increasing preload and, consequently, the difference between mean aortic pressure and mean left-ventricular intramural wall stress declines. With decreasing difference between mean aortic pressure and mean intramural wall stress, the coronary flow is reduced. This interplay between left-ventricular wall stress on the one hand and coronary flow on the other is expressed in the critical value of enddiastolic wall stress, at which a further increase in preload leads to a marked reduction in coronary flow and, hence, to a fall in the systolic wall stress parameters.

摘要

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