Metabolism of the acutely ischemic dog heart. II. Interpretation of a model

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Abstract
Glycolytic oscillations in an acutely ischemic dog heart were analyzed with a computer model. The major regulations of the glycolytic pathway flux occurred at phosphohexose isomerase, which is inhibited by accumulated pentose shunt intermediates; at phosphorylase, which shapes the 1st cycle of the oscillation; and at aldolase, which shapes the last 2 cycles. Aldolase is not under normal substrate control. Its activity and that of some subsequent glycolytic enzymes appear to be regulated by known interactions with the muscle proteins. The mitochondria become reduced as a result of anoxia and their metabolism reorganizes to export rather than import reducing equivalents. The behavior of this preparation can be explained in terms of the known metabolism of less severely perturbed hearts, especially (but not completely) in terms of effects of anoxia. The reasons for the inapplicability of the crossover theorem previously used to analyze this preparation are described.