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31P nuclear magnetic resonance (NMR) studies of creatine phosphokinase (CPK) kinetics using saturation transfer techniques are reported. The phosphocreatine (PCr) and adenosine triphosphate (ATP) levels in perfused hearts can be altered experimentally by stopping the flow of perusate (ischemia) to the heart for 35-min periods, followed by reperfusion to produce stable levels of performance. Utilization of energy by the heart was altered by administration of 25 mM potassium chloride (KCl) in the perfusate, which arrests contraction of the myocardium. Compared with control heart studies, the unidirectional rates measured during ischemia and KCl arrest are altered. The rates observed in the control experiments indicate that the CPK system is not in a steady state. This apparent deviation from steady-state conditions is ascribed to the existence of intracellular compartmentation of ATP.
Nunnally et al. (Wed,) studied this question.