Prostacyclin rather than endogenous nitric oxide is a tissue protective factor in myocardial ischemia
Woditsch, I.; Schrör, K.
American Journal of Physiology 263(5 Pt 2): H1390-H1396
1992
ISSN/ISBN: 0002-9513 PMID: 1443194 Document Number: 397174
Nitric oxide (NO) and prostacyclin (PGI-2) were determined in effluents of Langendorff-perfused rabbit hearts subjected to 2 h of global low-flow ischemia and subsequent reperfusion. PGI-2 release (6-oxo-prostaglandin (PG) F-1alpha) was significantly enhanced during early reperfusion and remained elevated. NO formation was reduced during ischemia but did increase substantially during reperfusion. Indomethacin (3 mu-M) significantly suppressed ischemia-related 6-oxo-PGF-1alpha and NO release. This was accompanied by severely diminished myocardial recovery. N-G-nitro-L-arginine (L-NNA) (100 mu-M) suppressed NO generation without major effects on 6-oxo PGF-1alpha generation and cardiac dysfunction but with a remarkable increase in coronary perfusion pressure. These effects of L-NNA were antagonized by L-arginine, whereas the effects of indomethacin were not. There was a substantial loss of creatine kinase specific activity from reperfused ischemic hearts, which was further aggravated by indomethacin but not by L-NNA. These data demonstrate a cardioprotective and endothelium-protective role of PGI-2 in myocardial ischemia, which also involves preservation of NO generation. Endogenous NO appears to be important for local regulation of coronary flow.