Anoxia induced release of prostaglandins in rabbit isolated hearts

Abstract

The relationship was investigated between prostaglandin release and the coronary vasodilatation 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 <1 ng/ml) in 60 of 66 hearts. This basal release was abolished by the prostaglandin synthetase inhibitor, indomethacin (1 to 2 μg/ml), a result which further adds to the identity of the prostaglandinlike substance as a prostaglandin. Anoxia increased coronary flow sometimes by 100% and evoked prostaglandin release shortly thereafter. Abolition of prostaglandin synthesis by indomethacin pretreatment did not affect nor did infusion of exogenous prostaglandin mimic the anoxia induced flow increment; thus, it is concluded that prostaglandin release cannot account for the anoxia induced vasodilatory response. Furthermore, the failure of indomethacin to after 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.