Role of PGF 2α in the superior mesenteric artery-induced shock

Abstract

The role of PGF 2α in circulatory shock of intestinal origin was investigated in anesthetized dogs by measuring PGF 2α levels in superior mesenteric vein, right ventricle, aorta, and femoral vein during superior mesenteric artery occlusion-induced shock by comparing the circulatory effects of exogenous PGF 2α injected into either the superior mesenteric or the femoral vein and by inhibiting of prostanoid synthesis with indomethacin. Release of the superior mesenteric artery occlusion caused a dramatic decrease in mean arterial blood pressure; an increase in mean portal venous pressure, and more than fivefold increases in plasma PGF 2α levels in superior mesenteric vein, right ventricle, and aorta. In spite of the decreased mean arterial blood pressure, postocclusion blood flow in the mesenteric artery did not fall below preocclusion values. Indomethacin in itself, significantly reduced plasma PGF 2α levels as well as intestinal blood flow and increased mean arterial blood pressure in animals without superior mesenteric artery occlusion. Furthermore, indomethacin attenuated the magnitude of postocclusion hypotension and completely prevented PGF 2α production during superior mesenteric artery occlusion shock. Exogenous PGF 2α 10 μg/kg injected into the superior mesenteric or femoral vein produced hypotension or hypertension, respectively. When PGF 2α was injected into the superior mesenteric vein, the plasma level of PGF 2α in the aorta was similar to that observed during superior mesenteric artery occlusion shock, whereas PGF 2α injected into the femoral vein gave a significantly higher concentration. Pulmonary metabolism of PGF 2α was significantly reduced in shock. The present results suggest that PGF 2α released by intestinal tissues might play an important role in shock caused by intestinal ischemia.