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succinate dehydrogenase/infarction

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This 16-year-old boy presented with acute retrosternal pain possibly representing acute myocardial infarction. Cardiac enzymes were within reference ranges. There were marked increases in metanephrine to 3299 μg/24 h (reference, <400 μg/24 h), normetanephrine to 1309 μg/24 h (reference, 0-390 μg/24
OBJECTIVE Previous studies demonstrated that pre-treatment with malonate, a reversible inhibitor of succinate dehydrogenase, given before ischaemia, reduces infarct size. However, it is unknown whether administration of malonate may reduce reperfusion injury. RESULTS Isolated mice hearts were
Inhibition of succinate dehydrogenase (SDH) with malonate during reperfusion reduces infarct size in isolated mice hearts submitted to global ischemia. However, malonate has toxic effects that preclude its systemic administration in animals. Here we investigated the effect of intracoronary malonate
The rate of oxidation of NADH and 3-hydroxybutyrate was studied in heart mitochondria after short-term (60 min) occlusion of coronary artery and the subsequent reperfusion. Addition of NAD increased the rate of 3-hydroxybutyrate oxidation, lowered in mitochondria of impaired tissue, but no complete
In consecutive medicolegal material comprising 79 persons, the formazan test revealed recent myocardial infarction in 16 cases (20%). Only 4 of these cases (25%) were demonstrated by macroscopic examination. By means of microscopic examination, the 4 infarctions recognized macroscopically and 5
A correction to this article has been published and is linked from the HTML and PDF versions of this paper. The error has been fixed in the paper.
Study of the effects of antioxidant therapy on the antioxidant defense enzymes and mitochondrial energy metabolism in patients with acute myocardial infarction showed that addition of antioxidants to therapeutic protocols promoted a sooner stabilization of the status of the patients and shortened

Reduction of myocardial infarct size in rats under the effect of bepridil.

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The ability of intravenous or oral bepridil to reduce infarct size was studied in the rat submitted in situ to coronary-artery ligation. Infarct size was measured by planimetry of serial 8-micron sections at known intervals 48 hr after left-coronary-artery ligation. Succinate dehydrogenase activity
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 response to exercise was investigated in trained and sedentary rats with moderate compensated heart failure produced by myocardial infarction (MI) and in rats that underwent sham operations. Trained rats ran on a treadmill (10% grade at 20 m/min) for 60 min/day, 5 days/week for 10 to 12 weeks,
The effects of revascularization on the morphological aspects of myocardial infarction have been studied in 87 animals. After permanent ligation of a coronary artery, the aspects are stereotyped and the histo-enzymatic and ultrastructural evolution is quite well known. On the contrary, early
Experiments on 107 rabbits and 76 white rats with the use of electrophysiological, biochemical and electron microscopy research methods have shown that nonachlazine-induced improvement of heart contractility in microfocal myocardial infarction occurs as a result of the shortening of the systolic and
Under conditions of experimental myocardium infarction caused in dogs by ligation of the anterior descending branch of the left coronary artery, the activity of alpha-ketoglutarate dehydrogenase and succinate dehydrogenase in mitochondria of the cortex, cerebellum and medulla ablongata lowers most
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
Myocardial infarction was induced in rats by ligating a coronary artery. During a week they received daily injections of 50 mg/kg of vitamin E intramuscularly or 30 mug/kg of sodium selenite subcutaneously, or else a combination of these preparations. The control animals received no injections.
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