Pulmonary and systemic vasodilator effect of the newly discovered prostaglandin PGI ₂

The effects of the newly discovered bicyclic prostaglandin, prostacyclin (PGI ₂), on the pulmonary and systemic vascular beds were investigated in the anesthetized dog. PGI ₂ decreased systemic and pulmonary arterial pressures in a dose-related manner when injected into the vena cava in doses of 1-30 μg. Since left ventricular end-diastolic, left atrial, and right atrial pressures were unchanged, and since cardiac output was increased or unchanged, pulmonary and systemic vascular resistances were decreased. PGI ₂ was 10 times more potent than prostaglandins E ₁ or E ₂ in decreasing aortic pressure when injected intravenously, and the effects of PGI ₂ on the systemic vascular bed were similar when injected into the vena cava or the left atrium. These data indicate that inactivation of PGI ₂ is minimal in the lung. The stable prostacyclin metabolite, 6-keto-PGF1α, had little hemodynamic efects, suggesting that responses to PGI ₂ were not due to formation of this metabolite. PGI ₂ produced dose-dependent increases in blood flow in the mesenteric and renal vascular beds. These data demonstrate that PGI ₂ has marked vasodilator activity in the pulmonary and systemic vascular beds and suggest that prostacyclin is the only known metabolite of arachidonic acid that dilates the pulmonary and systemic circulations.