title: Role of PGF2 alpha in the superior mesenteric artery-induced shock.
abstract: The role of PGF2 alpha in circulatory shock of intestinal origin was investigated in anesthetized dogs by measuring PGF2 alpha 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 PGF2 alpha 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 PGF2 alpha 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 PGF2 alpha 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 PGF2 alpha production during superior mesenteric artery occlusion shock. Exogenous PGF2 alpha 10 micrograms/kg injected into the superior mesenteric or femoral vein produced hypotension or hypertension, respectively. When PGF2 alpha was injected into the superior mesenteric vein, the plasma level of PGF2 alpha in the aorta was similar to that observed during superior mesenteric artery occlusion shock, whereas PGF2 alpha injected into the femoral vein gave a significantly higher concentration. Pulmonary metabolism of PGF2 alpha was significantly reduced in shock. The present results suggest that PGF2 alpha released by intestinal tissues might play an important role in shock caused by intestinal ischemia.
authors.affiliation: Department of Surgery III, Semmelweis University Medical School, Budapest, Hungary.
authors.forename: T
authors.initials: T
authors.lastname: Mózes
authors.forename: E
authors.initials: E
authors.lastname: Wieszt
authors.forename: T
authors.initials: T
authors.lastname: Zahajszky
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D015237:Dinoprost / Q000494:pharmacology / Q000502:physiology*; D004285:Dogs; D006439:Hemodynamics / Q000187:drug effects; D007213:Indomethacin / Q000494:pharmacology*; D007413:Intestinal Mucosa / Q000378:metabolism; D007422:Intestines / Q000098:blood supply; D007511:Ischemia / Q000503:physiopathology; D008638:Mesenteric Arteries; D008641:Mesenteric Vascular Occlusion / Q000503:physiopathology*; D012769:Shock / Q000503:physiopathology*
chemical_list: D015237:Dinoprost; D007213:Indomethacin