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. 1992:37:312-9.
doi: 10.1007/978-3-0348-7262-1_43.

Endogenous prostacyclin preserves myocardial function and endothelium-derived nitric oxide formation in myocardial ischemia

K Schrör  1 , I Woditsch
Affiliations

Endogenous prostacyclin preserves myocardial function and endothelium-derived nitric oxide formation in myocardial ischemia

K Schrör et al. Agents Actions Suppl. 1992.

Abstract

Nitric oxide (NO) and prostacyclin (PGI2) release was determined in effluents of Langendorff-perfused rabbit hearts under control conditions and during reperfusion subsequent to 2 h of global, low-flow ischemia. PGI2 release (6-oxo-PGF1 alpha) was significantly enhanced during early reperfusion and remained enhanced during a total time of 70 min of reperfusion. NO formation was reduced during ischemia but was substantially enhanced during reperfusion. Inhibition of endogenous PGI2 production by indomethacin resulted in severe disturbance of myocardial function and NO release. Inhibition of NO generation by L-N-nitroarginine did not affect myocardial contractility. These data suggest a cardioprotective and endothelium-protective role of PGI2 in myocardial ischemia which also involves protection of NO generation.

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