This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Taggart, J. V. Articles by LEE, K. S. Search for Related Content PubMed PubMed Citation Articles by Taggart, J. V. Articles by LEE, K. S.

(Circulation. 1961;24:416.)
© 1961 American Heart Association, Inc.

---

High Energy Phosphates and the Force of Contraction of Cardiac Muscle

John V. Taggart M.D.; ROBERT F. FURCHGOTT PH.D.¹; KWANG SOO LEE M.D., PH.D.¹

¹ From the Department of Pharmacology, State University of New York Downstate Medical Center, Brooklyn, New York.

This paper reviews studies performed by the authors and by others on the levels of high energy phosphate compounds—adenosine triphosphate (ATP), adenosine diphosphate (ADP), and creatine phosphate (CP)—of cardiac muscle under various conditions influencing contractile force. Interference with energy metabolism decreases both contractile force and high energy phosphates, especially CP. Certain types of experimental "failure" are associated with decreases in high energy phosphates; however, other types of "failure" occur without significant decreases in these phosphates. In addition, marked decreases or increases in contractile force, independent of significant changes in high energy phosphates, can be produced by drugs, by changes in heart rate, or by alterations in extracellular concentrations of cations. A decrease in force when levels of high energy phosphate are normal may be attributed to a deficiency in the utilization of these energy stores for mechanical work. The nature of this deficiency has been analyzed in isolated cat papillary muscles by simultaneously determining the activity oxygen consumption and contractile force per beat. In the case of decreases in contractile force due either to reduced heart rate or to spontaneous heart failure, the deficiency may be attributed almost completely to a loss in efficiency in the conversion of chemical energy in the high energy phosphates to mechanical energy (work). Cardiac glycosides, in restoring contractile force, do so by restoring the efficiency of this conversion. In the case of decreases in contractile force resulting from lowered extracellular Ca⁺⁺, the deficiency may be attributed partly to a loss of efficiency in this conversion and partly to a reduction in amount of high energy phosphate utilized per beat.

This article has been cited by other articles:

				M. A. Conway, P. A. Bottomley, R. Ouwerkerk, G. K. Radda, and B. Rajagopalan Mitral Regurgitation : Impaired Systolic Function, Eccentric Hypertrophy, and Increased Severity Are Linked to Lower Phosphocreatine/ATP Ratios in Humans Circulation, May 5, 1998; 97(17): 1716 - 1723. [Abstract] [Full Text] [PDF]

				E. J. Eichhorn and M. R. Bristow Medical Therapy Can Improve the Biological Properties of the Chronically Failing Heart: A New Era in the Treatment of Heart Failure Circulation, November 1, 1996; 94(9): 2285 - 2296. [Abstract] [Full Text]

				H. Yamakawa, M. Takeuchi, H. Takaoka, K. Hata, M. Mori, and M. Yokoyama Negative Chronotropic Effect of ß-Blockade Therapy Reduces Myocardial Oxygen Expenditure for Nonmechanical Work Circulation, August 1, 1996; 94(3): 340 - 345. [Abstract] [Full Text]

				Y. W. Cho, D. M. Aviado JR., and S. Bellet Myocardial Metabolic Changes During Acute Hemorrhage Angiology, September 1, 1965; 16(9): 532 - 537. [PDF]