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Am J Physiol Heart Circ Physiol 276: H1715-H1723, 1999;
0363-6135/99 $5.00
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Vol. 276, Issue 5, H1715-H1723, May 1999

Hypoperfusion-induced contractile failure does not require changes in cardiac energetics

Kurt W. Saupe1, Franz R. Eberli2, Joanne S. Ingwall3, and Carl S. Apstein1

1 Cardiac Muscle Research Laboratory, Boston University School of Medicine, Boston, Massachusetts 02118; 2 Kardiologie, Universitatsklinik, Inselspital, 3010 Bern, Switzerland; and 3 NMR Laboratory for Physiological Chemistry, Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115

Decreasing coronary perfusion causes an immediate decrease in contractile function via unknown mechanisms. It has long been suspected that this contractile dysfunction is caused by ischemia-induced changes in cardiac energetics. Our goal was to determine whether changes in cardiac energetics necessarily precede the contractile dysfunction as one would expect if a causal relationship exists. In 14 isolated rat hearts, we gradually decreased coronary perfusion using a coronary perfusate with a normal hematocrit and normal concentrations of the major metabolic substrates. Using 31P NMR spectroscopy to measure ATP, phosphocreatine (PCr), Pi, and ADP concentrations ([ATP], [PCr], [Pi], [ADP]), pH, and amount of free energy released from ATP hydrolysis (|Delta GATP|), we found that none of these variables changed significantly until several minutes after systolic pressure had significantly decreased. Even when developed pressure had decreased by over one-third, only very slight changes in [Pi], pH, and |Delta GATP| had occurred, with no significant changes in [ATP], [PCr], or [ADP]. Additionally, the rate of high-energy phosphate transfer between ATP and PCr did not decrease enough during hypoperfusion to explain the contractile dysfunction. We conclude that nonenergetic factors are the dominant cause of the initial decrease in systolic function when myocardial perfusion is decreased.

hibernation; ischemia; perfusion-contraction matching; metabolism


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