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Research Article Free access | 10.1172/JCI105734

Control of myocardial oxygen consumption: relative influence of contractile state and tension development

Thomas P. Graham Jr., James W. Covell, Edmund H. Sonnenblick, John Ross Jr., and Eugene Braunwald

Cardiology Branch, National Heart Institute, Bethesda, Maryland

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Cardiology Branch, National Heart Institute, Bethesda, Maryland

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Cardiology Branch, National Heart Institute, Bethesda, Maryland

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Cardiology Branch, National Heart Institute, Bethesda, Maryland

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Cardiology Branch, National Heart Institute, Bethesda, Maryland

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Published February 1, 1968 - More info

Published in Volume 47, Issue 2 on February 1, 1968
J Clin Invest. 1968;47(2):375–385. https://doi.org/10.1172/JCI105734.
© 1968 The American Society for Clinical Investigation
Published February 1, 1968 - Version history
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Abstract

Myocardial oxygen consumption was measured in 11 anesthetized, open-chest dogs in order to compare in the same heart the relative influence on oxygen usage of tension development and the contractile or inotropic state, as reflected in Vmax. the maximum velocity of shortening of the unloaded contractile elements. The isovolumetrically contracting left ventricle was studied with left ventricular volume, heart rate, and systemic perfusion rate controlled. Wall tension, contractile element velocity, and Vmax were calculated. Peak developed tension was increased at a constant Vmax by increasing ventricular volume, and the effect on oxygen consumption was determined. Oxygen utilization was then redetermined at an increased Vmax but at a constant peak developed tension by infusing norepinephrine (0.76 to 7.6 μg/min) and decreasing ventricular volume to match the tension existing before norepinephrine infusion. Oxygen consumption consistently increased with increases in both developed tension and Vmax with the following multiple regression equation relating these variables: myocardial oxygen consumption (μl/beat per 100 g in LV) = K + 0.25 peak developed tension (g/cm2) + 1.43 Vmax (cm/sec). These data indicate that the oxygen cost of augmentation of contractility is substantial, can be independent of any change in fiber shortening, and is similar in order of magnitude to the effect of alterations in tension development

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