Effect of indomethacin on coronary vascular response to increased myocardial oxygen consumption.
We tested the hypothesis that arachidonic acid metabolites mediate the coronary vascular response to changes in cardiac activity. Isoproterenol was administered intravenously to five chloralose-anesthetized, open-chest dogs. Left anterior descending coronary artery blood flow, systemic arterial blood pressure, and great cardiac vein O2 content were continuously measured, and blood gas determination (including O2 content) were made before and after infusions. From these data, coronary vascular conductance, coronary O2 delivery, and  myocardial O2 consumption were calculated. Isoproterenol increased conductance, O2 delivery, and O2 consumption. Indomethacin, a blocker of prostaglandin synthesis, was administered, and the isoproterenol infusions were repeated. The changes in conductance, O2 delivery, and O2 consumption associated with isoproterenol were not different after indomethacin was administered than before indomethacin was administered. Neither were the relations between conductance or O2 delivery and O2 consumption affected by indomethacin. We conclude that, in this preparation and with this stimulus, prostaglandins do not appear to mediate or modulate the coronary vascular response to changes in cardiac activity.
D000818:Animals; D001095:Arachidonic Acids / Q000494:pharmacology; D003326:Coronary Circulation / Q000187:drug effects*; D003331:Coronary Vessels / Q000502:physiology*; D004285:Dogs; D007213:Indomethacin / Q000494:pharmacology*; D007545:Isoproterenol / Q000494:pharmacology; D009206:Myocardium / Q000378:metabolism*; D010101:Oxygen Consumption; D011453:Prostaglandins / Q000096:biosynthesis / Q000502:physiology*
D001095:Arachidonic Acids; D011453:Prostaglandins; D007545:Isoproterenol; D007213:Indomethacin