INTRINSIC PROSTAGLANDIN RELEASE - MEDIATOR OF ANOXIA-INDUCED RELAXATION IN AN ISOLATED CORONARY-ARTERY PREPARATION

Abstract

Isolated coronary artery strips of the bovine heart in vitro relax in response to decreased bath O2 tensions (from 515 mm Hg to 112, 53 and 38 mm Hg). The rate of intrinsic formation and release of prostaglandin is considerably increased under conditions of decreased pO2 [O2 pressure]. The vascular relaxations under reduced pO2 are attenuated and the elevations in prostaglandin output blocked by prostaglandin synthesis inhibitors [aspirin, indomethacin and eicosa-5,8,11,14-tetraynoic- acid]. Alterations in the output of a PGE [prostaglandin E] with vasodilator activity, probably E1, is apparently a significant factor regulating the compensatory changes in tone of the coronary arteries in response to anoxic conditions.