succinate dehydrogenase/infarction

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Catecholamine-Induced Chest Pain Mimicking Infarction Due to an MIBG-Negative and DOPA-Positive Succinate Dehydrogenase Syndrome Subunit B-Related Pheochromocytoma.

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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

Succinate dehydrogenase inhibition with malonate during reperfusion reduces infarct size by preventing mitochondrial permeability transition.

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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

Selective Inhibition of Succinate Dehydrogenase in Reperfused Myocardium with Intracoronary Malonate Reduces Infarct Size.

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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

[Effect of experimental myocardial infarct on the succinate oxidation rate and succinate dehydrogenase activity in the heart mitochondria].

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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

The value of succinate dehydrogenase stain in the post-mortem diagnosis of early acute myocardial infarction. A forensic study.

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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

Author Correction: Selective Inhibition of Succinate Dehydrogenase in Reperfused Myocardium with Intracoronary Malonate Reduces Infarct Size.

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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.

[Effects of antioxidant therapy on the energy metabolism system and antioxidant defense during the acute period of myocardial infarction].

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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

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

Endurance training in rats with chronic heart failure induced by myocardial infarction.

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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,

[Membrane modifications in myocardial infarction following emergency reperfusion].

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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

[Effect of nonachlazine on the energy provision for cardiac contractile activity in experimental myocardial infarct].

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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

[Activity of enzymes of tricarboxylic and pentose-phosphate cycles in dog brain with myocardial infarction].

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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

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

[Morphologic indices the influence of selenium and vitamin E on the course of experimental myocardial infarct].

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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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