Oxygen deprivation and reoxygenation augment prostacyclin synthesis in cultured ventricular myocytes

Arié Pinson; Régine Tirosh; Victoria Tremblover; Esther Shohami

doi:10.1016/S0952-3278(96)90019-8

Oxygen deprivation and reoxygenation augment prostacyclin synthesis in cultured ventricular myocytes

Arié Pinson^*, Régine Tirosh, Victoria Tremblover, Esther Shohami

^*Corresponding author for this work

School of Pharmacy

Research output: Contribution to journal › Article › peer-review

3 Scopus citations

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 PGI₂) was found during 'ischemia', which continued to increase markedly during reoxygenation. PGE₂ levels were pronouncedly enhanced during ischemia but decreased during reoxygenation, and TXB₂ 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 PGI₂ and PGE₂ during ischemia and reoxygenation.

Original language	English
Pages (from-to)	211-215
Number of pages	5
Journal	Prostaglandins Leukotrienes and Essential Fatty Acids
Volume	54
Issue number	3
DOIs	https://doi.org/10.1016/S0952-3278(96)90019-8
State	Published - 1996

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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 PGI2) was found during 'ischemia', which continued to increase markedly during reoxygenation. PGE2 levels were pronouncedly enhanced during ischemia but decreased during reoxygenation, and TXB2 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 PGI2 and PGE2 during ischemia and reoxygenation.",

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AU - Tirosh, Régine

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Oxygen deprivation and reoxygenation augment prostacyclin synthesis in cultured ventricular myocytes

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