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Circulation Research. 1966;19:221-229

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(Circulation Research. 1966;19:221.)
© 1966 American Heart Association, Inc.

Myocardial High Energy Phosphate Stores in Acutely Induced Hypoxic Heart Failure

PETER E. POOL M.D.1, JAMES W. COVELL M.D.1, CHARLES A. CHIDSEY M.D.1, EUGENE BRAUNWALD M.D.1

1 Cardiology Branch, National Heart Institute, Bethesda, Maryland

In order to determine the relation between depression of myocardial function and the myocardial high energy phosphate stores during acute hypoxia, a technique for serial evaluation of these stores was developed. Acute hypoxia was induced in 18 anesthetized dogs and serial determinations of adenosine triphosphate (ATP) and creatine phosphate (CP) were made while myocardial function was continuously measured. Myocardial concentrations of ATP were maintained even in the presence of severe hypoxia and myocardial failure. There was a small depression of the average myocardial CP concentration during early heart failure. However, in more than one-third of the dogs there was no significant depression of CP concentration at this time. It is concluded that hypoxic depression of myocardial function is not initiated by a decrease in the total myocardial high energy phosphate stores. The possibility could not be excluded that a particular fraction of the high energy phosphate store is decreased when myocardial failure is induced by hypoxia.


Key Words: adenosine triphosphate • creatine phosphate • myocardial contractility • ventricular function • anoxia • cardiac depression • anesthetized dogs

Accepted on February 23, 1966




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