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.