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malate/infarzierung
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[Malate dehydrogenase isoenzymes in myocardial infarction].
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Plasma CPK activity and the activity of isoenzymes MDH, AST and LDH were assessed in 60 patients with myocardial infarction of different severity, with reference to the time since the onset of the attack. The peaks of CPK and MDH-C activity were reached sooner than those of LDH-M and AST-C, while
[Diagnostic and prognostic value of determining lactate and malate dehydrogenase activity in acute myocardial infarct].
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[The diagnostic importance of determining serum malate dehydrogenase and lactate dehydrogenase activity in patients with macrofocal myocardial infarct and angina pectoris].
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[The effect of alpha-ketoglutarate, malate and alpha-glycerophosphate on bioenergetic processes in ischemic myocardium].
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Anti-ischemic action of exogenous natural metabolites and their effect on biological combustion processes indexes in cardiac muscle has been investigated on white rats with the experimental myocardial infarction. It has been established that the marked cardioprotective effect of malate and
Infarct-remodelled hearts with limited oxidative capacity boost fatty acid oxidation after conditioning against ischaemia/reperfusion injury.
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OBJECTIVE
Infarct-remodelled hearts are less amenable to protection against ischaemia/reperfusion. Understanding preservation of energy metabolism in diseased vs. healthy hearts may help to develop anti-ischaemic strategies effective also in jeopardized myocardium.
RESULTS
Isolated
Changes in ECG and enzyme activity in rat heart after myocardial infarction: effect of TPP and MnCl2.
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Heart infarction is one of the main causes of death in the human population. Assurance of a sufficient level of bioenergetic processes is very important for the heart after infarction. Mn2+ as well as thiamine pyrophosphate (TPP) are positive effectors of the pyruvate dehydrogenase complex (PDH) and
Effect of alpha-tocopherol on mitochondrial electron transport in experimental myocardial infarction in rats.
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The effect of alpha-tocopherol pretreatment (6 mg/100 g body wt/day, orally for a period of 90 days) on mitochondrial electron transport in myocardial infarction induced by isoproterenol (20 mg/100 g body wt, subcutaneously for two days) was studied in rats. A significant decrease was observed in
ACE inhibition prevents myocardial infarction-induced skeletal muscle mitochondrial dysfunction.
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Heart failure is associated with alterations in cardiac and skeletal muscle energy metabolism resulting in a generalized myopathy. We investigated the molecular and cellular effects of angiotensin-converting enzyme inhibition (ACEi) on skeletal muscle metabolism in infarcted animals. Myocardial
Experimental coronary artery occlusion. I. Measurement of infarct size.
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We studied the size of infarcts in 25 dogs 48 hrs after proximal occlusion of the left anterior descending coronary artery. In one group of animals infarct size was measured by histologic criteria, in another group the infarct was measured macrohistochemically using p-NBT and malate to incubate
[Morphological changes in the lungs in myocardial infarct].
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Morphologica lesions in the lungs were studied in 48 rabbits with experimental myocardial infarction and in 17 fatal cases where death occurred at various intervals after the onset of myocardial infarction. The study revealed 4 interrelated stages of morphological lesions in the lungs due to the
Protective Effects of L-Malate against Myocardial Ischemia/Reperfusion Injury in Rats.
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Objective. To investigate the protective effects of L-malate against myocardial ischemia/reperfusion (I/R) injury in rats. Methods. Male Sprague-Dawley rats were randomly assigned to the following groups: sham (sham), an ischemia/reperfusion (I/R) model group (model), an DMF pretreated group (DMF),
Arbutin prevents alterations in mitochondrial and lysosomal enzymes in isoproterenol-induced myocardial infarction: An in vivo study
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The present study demonstrated the protective effects of arbutin (ARB) on hyperlipidemia, mitochondrial, and lysosomal membrane damage and on the DNA damage in rats with isoproterenol (ISO)-induced myocardial infarction (MI). Rats were pretreated with ARB (25 and 50 mg/kg body weight (bw)) for 21
[Cardioprotective effect of carnitine and its synthetic analog 3-(2,2,2-trimethylhydrazinium) propionate in rats with experimental myocardial infarction].
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Effect of carnitine and its synthetic analogue 3-(2,2,2-trimethylhydrazinium) propionate (THP) has been studied in rats with experimental infarction of myocardium following occlusion of the left anterior descending coronary artery. Morphological and biochemical changes were determined within 24 hrs
Matrix metalloproteinases and membrane damage markers in sera of patients with acute myocardial infarction.
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Coronary artery disease is a multifunctional disease and represents one of the leading causes of death worldwide. Oxidative stress appears as an etiological factor for myocardial damage during acute myocardial infarction. Some data suggest that acute coronary syndromes may also be influenced by
Altered plasma concentrations of glutamate, alanine and citrate in the early phase of acute myocardial infarction in man.
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Plasma levels of glutamate, alanine, free fatty acids (FFA), citrate, glucose, insulin, lactate, creatine kinase and aspartate aminotransferase were determined frequently during the first 2-48 h after onset of chest pain in 10 patients who developed acute myocardial infarction (AMI) and in 8 who did
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