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Research Article Free access | 10.1172/JCI107710

Coronary Hemodynamics and Regional Myocardial Metabolism in Experimental Aortic Insufficiency

Douglas M. Griggs Jr. and Chin Chi Chen

1Department of Physiology, University of Missouri Medical School, Columbia, Missouri 65201

Find articles by Griggs, D. in: PubMed | Google Scholar

1Department of Physiology, University of Missouri Medical School, Columbia, Missouri 65201

Find articles by Chen, C. in: PubMed | Google Scholar

Published June 1, 1974 - More info

Published in Volume 53, Issue 6 on June 1, 1974
J Clin Invest. 1974;53(6):1599–1606. https://doi.org/10.1172/JCI107710.
© 1974 The American Society for Clinical Investigation
Published June 1, 1974 - Version history
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Abstract

Acute aortic valvular insufficiency was induced in open chest dogs by employing a special intravascular cannula, or by rupturing an aortic valve leaflet. Phasic and mean coronary flow were assessed in some animals, while in others data were obtained on arterial and coronary sinus blood lactate, pyruvate, PO2, PCO2, and pH, and on myocardial tissue lactate, pyruvate, and water content in the outer and inner halves of the free wall of the left ventricle. Results showed that in acute aortic insufficiency diastolic coronary flow decreased as a function of aortic diastolic pressure, but systolic coronary flow increased in such proportion that mean coronary flow did not decrease. With moderate reductions in aortic diastolic pressure due to aortic insufficiency, myocardial blood flow was judged to be nutritionally adequate in both the outer and inner regions of the left ventricle. With more severe reductions in aortic diastolic pressure, the inner region exihibited biochemical signs of anaerobic metabolism. The presence of these metabolic changes could be correlated with either of two previously described pressure indexes. These findings suggest that the reduced coronary perfusion pressure and the intramyocardial tissue pressure gradient can be compensated for by autoregulation in some cases of aortic insufficiency, but in others such compensation may be incomplete, in which case oxygen delivery to the subendocardium will be inadequate to meet local tissue oxygen needs.

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