Hypoxia-induced prostaglandin release from rabbit heart.
Rabbit hearts were perfused at a pressure of 60 cm H2O with 37 degrees C Tyrode solution aerated with 5% CO2 in O2. The effluent from the heart was collected in four consecutive 10-min periods. The samples were analyzed for prostaglandins of the E series (PGE), using thin layer chromatography for identification and assay on the superfused rat stomach strip for quantitative estimation. Three different series of experiments were performed, the hearts in each series during the second effluent collection period being perfused under conditions of either hypoxia (Tyrode solution aerated with 5% O2 and 5% CO2 in N2), absence of glucose in the Tyrode solution, or hypotension/low perfusion flow (perfusion pressure lowered to 30cm H2O). In the series where glucose was omitted or hypotension/low perfusion flow was induced during the second effluent collection period, the outflow of PGE decreased exponentially throughout the four periods. In the series where hypoxia was maintained during the second effluent collection period, a marked increase in the outflow of PGE was noted after the end of hypoxia. Prostaglandins of the E series are powerful vasodilators, and the PG released may, by inducing coronary vasodilation, counteract the hypoxia. However, it has been shown that, in human plasma, conversion of arachidonic acid to PGE is parallelled by platelet aggregation. Therefore, if PG synthesis is also stimulated by hypoxia in man, myocardial ischemia must be considered as a possible mechanism for platelet aggregation and subsequent coronary thrombosis.
D000818:Animals; D003327:Coronary Disease / Q000378:metabolism; D005260:Female; D007003:Hypoglycemia / Q000378:metabolism; D007022:Hypotension / Q000378:metabolism; D000860:Hypoxia / Q000378:metabolism*; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D010477:Perfusion; D011453:Prostaglandins / Q000378:metabolism*; D011817:Rabbits
D011453:Prostaglandins