glutamate dehydrogenase/infarkt

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Morphology and mitochondrial function of the surviving myocardium following myocardial infarction in the cat.

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The surviving myocardium of the cat was studied 7 days and 6 weeks following experimental infarction. Seven days after infarction, ultrastructural alterations of the mitochondria indicative of slight hypoxic injury--clearing of the matrix and loss of dense matrix granules--were found. Together with

Systemic short-term fibrinolysis with high-dose streptokinase in acute myocardial infarction: time course of biochemical parameters.

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The course of plasma catalytic activities of total creatine kinase, creatine kinase isoenzyme MB, total, cytoplasmatic and mitochondrial aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase, alpha-hydroxybutyrate dehydrogenase, glutamate dehydrogenase and concentrations of

[Enzyme diagnosis of liver dysfunction in acute myocardial infarct and its complications].

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A complex of enzymatic tests, characterizing the liver function and cellular cytolysis in patients with acute myocardial infarction of various severities (without complications and with various types of complications and outcomes) was used in examinations over the first week of the disease.

[Histochemical data on changes of various indicators of protein metabolism in the myocardium beyond the infarct zone].

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Changes in some values of protein metabolism in the heart muscle (the activity of myosin ATPase, leucilaminopeptidase, glutamate dehydrogenase, as well as the content of SH-groups, urea, RNA and DNA) were studied by histochemical methods in the parts of the myocardium remote from the zone of the

Ischemic tolerance in an in vivo model of glutamate preconditioning.

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Ischemia initiates a complicated biochemical cascade of events that triggers neuronal death. This study focuses on glutamate-mediated neuronal tolerance to ischemia-reperfusion. We employed an animal model of lifelong excess release of glutamate, the glutamate dehydrogenase 1 transgenic (Tg) mouse,

Serial changes in cytosolic, mitochondrial, and lysosomal enzymes and cardiac myosin light chain II in plasma following coronary ligation in conscious closed-chest dogs.

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We studied serial changes in various myocardial enzymes and cardiac myosin light chain II (LCII) in plasma following coronary ligation in 14 conscious closed-chest dogs. Cytoplasmic enzymes [creatine phosphokinase (CPK) and supernatant glutamic oxaloacetic transaminase (sGOT)] reached maximum at

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