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ionol/necrotisch
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8 resultaten
[Limitation of ischemic necrosis by the use of antioxidant ionol].
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Inhibitory effect of Ionol on lipid peroxidation (LPO) in the infarction zone and out of it after experimental myocardial infarction in the experiments on rats was investigated. The results of measurements, performed by two independent methods: point counting and the computer image analysis were
[Comparative study of the effect of alpha-tocopherol, its synthetic metabolite and ionol on dexamethasone-induced apoptosis in rat thymocytes].
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alpha-Tocopherol was found to decrease the level of rat thymocytes DNA fragmentation and to increase the viability of these cells under apoptosis induction by dexamethazone. So the antiapoptotic role of this vitamin is suggested. In contrast to alpha-tocopherol synthetic antioxidant ionol and
Disturbances of the heart structure and function in chronic hemolytic anemia, their compensation with increased coronary flow, and their prevention with ionol, an inhibitor of lipid peroxidation.
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The structure and function of heart muscle were studied in rats with chronic hemolytic anemia induced by phenylhydrazine. Contractural lesions, myocytolysis, fatty dystrophy, and small-focal necrosis were found in the myocardium along with hypertrophy. The disturbances were accompanied by a
[Myocardium damage in experimental anemia and its prevention with the antioxidant ionol].
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Rats with hemolytic (phenylhydrazine) anemia were shown to develop simultaneously with hypertrophy of the myocardium marked damages of cardiomyocytes of the type of I-III degree contractures, myocytolysis, vacuolation, fatty infiltration, small focal necrosis as well as a peculiar form of damages
[Role of monoaminoxidase in the intensification of peroxidation of lipids in mitochondria during experimental myocardial necrosis].
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The relationship between lipid peroxidation and rat heart mitochondrial monoamine oxidase activity was studied in experimental myocardial necrosis induced by adrenaline injection. It has been established that both the intensity of peroxidation and the activity of monoamine oxidase in mitochondria
[Prevention of myocardial damage during hemolytic anemia by antioxidants].
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Structural and functional disorders of the heart muscle were studied in rats with phenylhydrazine-induced chronic hemolytic anemia, as was the possibility of their prevention with anti-oxidant Ionol, a lipid peroxidation inhibitor. Hemolytic anemia was shown to produce myocardial contractural
[Metabolic bases of the pathogenesis of severe multiple trauma].
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Under analysis there were data of hormonal activity of the hypothalamo-hypohysis-adrenocortical system and the incretory apparatus of the pancreas, metabolism (of proteins, lipids, carbohydrates) and concentration of microelements (iron, zinc), lipid peroxidation (content of malonic dialdehyde and
Beta-catenin in the fibroproliferative response to acute lung injury.
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Resolution of alveolar epithelial/capillary membrane damage after acute lung injury requires coordinated and effective tissue repair to reestablish a functional alveolar epithelial/capillary membrane barrier. We hypothesized that signaling pathways important in lung alveolar bud ontogeny are
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