Arachidonic acid in splanchnic artery occlusion shock.

Arachindonic acid infused into the mesenteric vascular bed of normal pentobarbital-anesthetized dogs at a concentrations of 150 mug/kg per min produced no significant changes in mean arterial blood pressure (MABP), portal vein pressure (PVP), screen filtration pressure (SFP), platelet count, circulating lysosomal enzyme or myocardial depressant factor (MCF) activities, nad only modestly increased superior mesenteric arter flow (SMAF)ans endogenous prostaglandin concentrations concentrations. It is concluded that arachidonic acid, at the infusion rate employed, dose not have any major effect on the circulatory status or on the lysosomal or platelet stability in normal dogs. In contrast, arachidonic acid administered to dogs in splanchnic artery occulusion (SAO) shock significantly exacerbated the decline in MABP seen after release of the occlusive clamps and also significantly reduced mesenteric blood flow. The hypothnsive of arachidonic acid appears to be partly due to the fatty acid itself and partly due to the metavolically formed prostaglandin endoct the platelet count or aggregability, lysosomal hydrolase activity, or MDF formation in the SAO shock dogs. These data suggest that increased endogenous prostaglandin concentrations in themselves are not a prime factor in the pathophysiology of circulatory shock, but that endogenous prostaglandin or related substances can significantly modulate the shock state.