Increase in the coronary vascular resistance by indomethacin in the isolated guinea pig heart preparation in the absence of changes in mechanical performance and oxygen consumption.
Experiments were performed in isolated guinea pig hearts, perfused at constant volume. Left ventricular pressure, left ventricular dp/dtmax, coronary vascular pressure and coronary venous pO2 were measured continuously. Indomethacin (1.4 X 10(-6) M) increased coronary vascular resistance by 15% over control (p less than 0.01) without altering the myocardial contractile force. When PGE2 (1.4 X10(-8) M) was subsequently added, it abolished the indomethacin action and lowered the coronary vascular resistance below the pre-indomethacin control value. This increase in coronary vascular resistance caused by indomethacin was also seen when the animals were pretreated with reserpine and/or the adrenoceptor blocking agents phenoxybenzamine and propranolol, but was prevented completely by previous addition of PGE2 (1.4 X 10(-7) M). The results provide evidence for possible involvement of endogenous prostaglandin-like substances in the maintenance of coronary vascular resistance in the isolated guinea pig heart.
D000818:Animals; D003331:Coronary Vessels / Q000187:drug effects*; D005260:Female; D006168:Guinea Pigs; D006439:Hemodynamics / Q000187:drug effects*; D066298:In Vitro Techniques; D007213:Indomethacin / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects; D010101:Oxygen Consumption / Q000187:drug effects*; D010643:Phenoxybenzamine / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D011458:Prostaglandins E / Q000494:pharmacology; D012110:Reserpine / Q000494:pharmacology; D013268:Stimulation, Chemical; D014439:Tyramine / Q000494:pharmacology; D014655:Vascular Resistance / Q000187:drug effects*
D011458:Prostaglandins E; D010643:Phenoxybenzamine; D012110:Reserpine; D011433:Propranolol; D014439:Tyramine; D007213:Indomethacin