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malate dehydrogenase/infarction

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LidwoordKlinische proevenOctrooien
Bladzijde 1 van 21 resultaten

[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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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
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
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
BACKGROUND Myocardial infarction is a public health problem. Functional food is an alternative treatment for cardiovascular diseases. OBJECTIVE The objective was to analyze the functional and anatomopathological post-myocardial-infarction effects of soybean extract (SE) and isoflavone
Dietary flavonoids intake has been reported inversely related to the incidence of cardiovascular diseases (CVD). The present study is undertaken to evaluate the preventive role of naringin on mitochondrial enzymes in isoproterenol (ISO)-induced myocardial infarction in male albino Wistar rats. Rats
Altered mitochondrial function and free radical-mediated tissue damage have been suggested as an important pathological event in isoproterenol (ISO)-induced cardiotoxicity. This study was undertaken to know the preventive effect of morin on mitochondrial damage in ISO-induced cardiotoxicity in male
The present study investigates the effect of aspartate and glutamate on mitochondrial function during myocardial infarction (MI) in wistar rats. Male albino wistar rats were pretreated with aspartate [100 mg(kgbody weight)(-1) day(-1)] or glutamate [100 mg(kg body weight)(-1) day(-1)]
With recent advances in nutrition sciences, natural products and health-promoting foods have received extensive attention from both health professionals and the common population. The flavonoid rich fraction (FRF) of Dioscorea bulbifera Linn. has a strong free radical scavenging activity. FRF (150
Asperosaponin VI is a saponin of the medicinal herb Dipsacus asper (Xuduan), and no pharmacological activity has been reported yet. In this study, we investigated the anti-myocardial ischemia effects of Asperosaponin VI (ASA VI) both in vivo and in vitro. An animal model of myocardial ischemia(MI)

Skeletal muscle oxidative capacity and exercise tolerance in rats with heart failure.

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OBJECTIVE Past research has shown the development of exercise intolerance after myocardial infarction (MI). The purpose of this study was to test the hypothesis that reductions in oxidative enzyme activity, in a variety of skeletal muscles, coincide with the development of exercise intolerance in a
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