Abstract
Prostacyclin production in cultured cardiomyocytes is not induced by cellular ATP depletion per se, suggesting that the mechanism of ischemic injury is more complex. In the present study we subjected cultured ventricular myocytes to ‘simulated ischemia’ followed by reoxygenation. A slight increase in 6-keto-PGF 1α (the stable metabolite of PGI 2) was found during ‘ischemia’, which continued to increase markedly during reoxygenation. PGE 2 levels were pronouncedly enhanced during ischemia but decreased during reoxygenation, and TXB 2 levels remained undetectable throughout. These findings reflect a cardiomyocyte response to anoxic injury, suggesting that they act to protect against cardiac injury by producing the potent vasodilators PGI 2 and PGE 2 during ischemia and reoxygenation.
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