title: Anoxia-induced release of prostaglandins in rabbit isolated hearts.
abstract: We investigated the relationship between prostaglandin release and the coronary vasodilation evoked by anoxia. Isolated rabbit hearts were perfused via the aorta with Krebs-Ringer's solution. The coronary effluent was bioassayed continuously in terms of prostaglandin E2 for prostaglandinlike substance which was present (at less than 1 ng/ml) in 60 of 66 hearts. This basal release was abolished by the prostaglandin synthetase inhibitor, indomethacin (1-2 mug/ml), a result which adds further to the identity of the prostaglandinlike substance as a prostaglandin. Anoxia increased coronary flow sometimes by 100% and evoked prostaglandin release shortly thereafter. Ablolition of prostaglandin synthesis by indomethacin pretreatment did not affect nor did infusion of exogenous prostaglandin mimic the anoxia-induced flow increment; thus, we conclude that prostaglandin release cannot account for the anoxia-induced vasodilator response. Furthermore, the failure of indomethacin to alter resting coronary blood flow suggests that a local prostaglandin release is not responsible for either the maintenance or the modulation of coronary flow in this preparation.
mesh_terms: D000818:Animals; D003326:Coronary Circulation; D006940:Hyperemia; D000860:Hypoxia / Q000378:metabolism*; D007213:Indomethacin / Q000494:pharmacology; D009206:Myocardium / Q000378:metabolism*; D011448:Prostaglandin Antagonists; D011453:Prostaglandins / Q000378:metabolism*; D011817:Rabbits
chemical_list: D011448:Prostaglandin Antagonists; D011453:Prostaglandins; D007213:Indomethacin