Mechanism of cardiac damage in anoxia

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Abstract
The following hypothesis is suggested to explain the mechanism of anoxic damage in cardiac tissue. Lactic acid accumulation, resulting from anoxia, overcomes the buffer capacity of the sarcoplasm. The consequent increased intracellular acidity leads to activation of proteolytic enzymes in the heart tissue and thus to destruction of apoenzyme protein and disruption of metabolic systems. To test this hypothesis and gain information concerning the well-known resistance of infant tissue to anoxia, adult and infant rat heart muscle was subjected to determinations of lactic acid production in anoxia, buffer capacity and proteolytic activity. Results show that a cathepsin is present in heart tissue which is active only at pH levels below 5 and is almost twice as active in adult heart as in infant. Lactic acid accumulates in both infant and adult anoxic heart, but more rapidly in the latter, and in both is accompanied by intracellular proteolysis. It is suggested that these findings are in consonance with the hypothesis, although certain discrepancies from the predicted results are noted.