Prostacyclin produced by the pericardium and its influence on coronary vascular tone

To determine the influence of pericardial fluid prostacyclin on coronary blood flow, the latter was measured in the circumflex artery of anesthetized dogs. Intraaortic infusions of angiotensin II (25 ng . kg-1 . min-1) reduced blood flow and released prostacyclin into pericardial fluid. Epicardial and pericardial superfusion with indomethacin (1 micrograms/ml) abolished prostacyclin release and significantly increased the coronary vasoconstrictor effect of angiotensin II; this treatment did not appear to affect vascular synthesis of prostacyclin. Pericardial prostacyclin may modulate the coronary vasoconstrictor effect of angiotensin, but its general role as a regulator of coronary vascular resistance is probably limited. A more important effect of pericardial prostacyclin may be exerted on the large coronary vessels in the epicardial surface. Release of prostacyclin into pericardial fluid represents a potential mechanism for opposing coronary vasospasm, especially if platelet activation is found to be a contributory factor in vasotonic angina pectoris.