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.
|Original language||English (US)|
|Number of pages||6|
|Journal||Journal of Applied Physiology Respiratory Environmental and Exercise Physiology|
|State||Published - Dec 1 1978|
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