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AJP - Heart and Circulatory Physiology, Vol 258, Issue 1 9-16, Copyright © 1990 by American Physiological Society
ARTICLES |
Y. Koretsune and E. Marban
Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205.
When coronary perfusion is interrupted, the diastolic force generated by the myocardium first falls but eventually increases. The delayed rise in force, ischemic contracture, has been attributed either to ATP depletion or to elevation of the intracellular free calcium concentration ([Ca2+]i). To distinguish between these possibilities, we measured [Ca2+]i and ATP concentration [( ATP]) in ferret hearts using nuclear magnetic resonance (NMR) spectroscopy. Mean time-average [Ca2+]i and [ATP] equaled 0.25 microM and 2.7 mumol/g wet wt, respectively, under control perfusion conditions. [Ca2+]i increased and [ATP] fell during total global ischemia. Although [Ca2+]i exceeded the usual systolic levels of 1.7 microM within 20-25 min of ischemia and reached a steady level between 2 and 3 microM by 30-35 min, force only began to rise after 40 min. In contrast, the time required for [ATP] to fall to less than 10% of control levels coincided closely with the onset of contracture. Ischemia in the presence of iodoacetate, an inhibitor of glycolysis, led to a precipitous fall in [ATP] and a concomitant rise in force, both of which preceded any elevation of [Ca2+]i. Thus changes in [Ca2+]i are neither sufficient nor necessary for the initiation of ischemic contracture. We conclude that ATP depletion is primary and that the rise in resting force reflects the formation of rigor cross bridges.
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