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Search for: [Abstract = "The objective of this study was to characterize MNA\+ endothelial function in animal models. I used two animal models of endothelial dysfunction\: a streptozotocin\-induced diabetes model and a model of hypertriglyceridemia induced by high\-fructose diet. I also used two models for in vitro study\: a model of pyrogallolinduced endothelial impairment in isolated aorta of a rat and a model of endothelial impairment induced by hydrogen peroxide in the cell line EA. hy926. In the first model endothelial impairment was observed only as the endothelial impairment of NO\-dependent vasodilation function, in the second model as a LDH release. Both in diabetes and in hypertriglycerydemia prolonged MNA\+ administration \(100 mg\/kg per. os.\) increased the level of endogenous MNA\+ and its metabolites in plasma. It prevented also endothelial dysfunction development \(the endothelium\-dependent relaxation dysfunction of aorta induced by acetylcholine and histamine\). In diabetes MNA\+ therapy did not reverse the PGI2 production by aortic wall although it prevented compensatory increase of 6\-keto\-PGF1a concentration in plasma. In hypertriglycerydemia, on the other hand, MNA\+ administration seemed to increase PGI2 production by vascular wall. MNA\+ decreased the level of triglycerides concentration in hypertriglyceridemic model however, this effect was not observed in diabetes model. In diabetes model MNA\+"]

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