4 Αποτελέσματα
Long-term impairments of energy metabolisms in myocardium were found in rats after clinical death caused by acute hemorrhage. Bioenergetics of myocardium tended to normalize within a month after resuscitation. Severity of postresuscitation period correlated with the level of deteriorations observed
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
One-hour ischemia followed by rat liver reoxygenation brings about the accumulation of endogenous products of lipid peroxidation (LPO) and deterioration of the monooxygenase system (the drop of cytochrome P-450 content, amidopyrine N-demethylase and NADP X H cytochrome reductase activity).
Acute hypoxia was accompanied by intensification of lipid peroxidation in synaptosomal and mitochondrial rat brain fractions as well as by inhibition of Na+, K+- and Mg2+-ATPases. Preadministration of antioxidants vitamin E and ionol into animals prevented distinctly the increase in lipid