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Arachidonic acid in splanchnic artery occlusion shock



Arachidonic acid in splanchnic artery occlusion shock



American Journal of Physiology 231(1): 112-119



Arachidonic acid infused into the mesenteric vascular bed of normal pentobarbital-anesthetized dogs at a concentration of 150 .mu.g/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 (MDF) activities, and only modestly increased superior mesenteric artery flow (SMAF) and endogenous prostaglandin concentrations. Arachidonic acid, at the infusion rate employed, does 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 occlusion (SAO) shock significantly exacerbated the decline in MABP seen after release of the occlusive clamps and also significantly reduced mesenteric blood flow. The hypotensive effect of arachidonic acid appears to be partly due to the fatty acid itself and partly due to the metabolically formed prostaglandin endoperoxides or native prostaglandins. However, arachidonic acid did not significantly affect the platelet count or aggregability, lysosomal hydrolase activity or MDF formation in the SAO shock dogs. Increased endogenous prostaglandin concentrations in themselves are not a prime factor in the pathophysiology of circulatory shock, but endogenous prostaglandins or related substances can significantly modulate the shock state.

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Accession: 004776579

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PMID: 961849



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