Effects of prostacyclin on systemic and coronary hemodynamics in the dog

The hemodynamic effects of intravenous and intracoronary prostacyclin (PGl2) were evaluated in anesthetized, open-chest instrumented dogs. Coronary artery and aortic blood flows, aortic and left ventricular (LV) diastolic pressure, and heart rate were measured continuously. With intravenous PGl2 both left anterior descending (LAD) and circumflex (LCX) coronary artery blood flows remained unchanged; both arterial and LV diastolic pressures declined; coronary resistance declined progressively with increasing PGl2; peak reactive hyperemic flow following 10-second coronary artery occlusion declined progressively with increasing PGl2; heart rate responses were variable at low doses but increased at high dose; and aortic blood flow increased consistently. With intracoronary PGl2 both LAD and LCX coronary blood flows increased promptly in dose-related manner. In dogs with critical coronary artery narrowing (loss of reactive hyperemia) created by an external plastic occluder, intravenous prostacyclin (0.5 μg/kg/min) did not after flow in the narrowed coronary artery, but increased flow in the non-narrowed coronary artery (p < 0.02) as both systemic arterial and LV diastolic pressures declined. These results show that PGl2 has potent direct coronary and systemic vasodilator actions.