Endogenous prostacyclin preserves myocardial function and endothelium-derived nitric oxide formation in myocardial ischemia.
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.
Schrör
K
K
Institut für Pharmacokologie, Heinrich-Heine-Universität Düsseldorf, FRG.
Woditsch
I
I
D000818:Animals; D001120:Arginine / Q000031:analogs & derivatives / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects; D003326:Coronary Circulation / Q000187:drug effects; D003327:Coronary Disease / Q000378:metabolism / Q000503:physiopathology*; D003402:Creatine Kinase / Q000378:metabolism; D011464:Epoprostenol / Q000502:physiology*; D006321:Heart / Q000502:physiology*; D006334:Heart Function Tests; D066298:In Vitro Techniques; D007213:Indomethacin / Q000378:metabolism; D009200:Myocardial Contraction / Q000187:drug effects; D015425:Myocardial Reperfusion; D009206:Myocardium / Q000201:enzymology; D009569:Nitric Oxide / Q000096:biosynthesis* / Q000378:metabolism*; D019335:Nitroarginine; D011817:Rabbits
D019335:Nitroarginine; D009569:Nitric Oxide; D001120:Arginine; D011464:Epoprostenol; D003402:Creatine Kinase; D007213:Indomethacin