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Neuroprotection conferred by post-ischemia ethanol therapy in experimental stroke: an inhibitory effect on hyperglycolysis and NADPH oxidase activation.

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Ethanol provides neuroprotection following ischemia/reperfusion. This study assessed ethanol's effect on hyperglycolysis and NADPH oxidase (NOX) activation. Adult, male Sprague-Dawley rats were subjected to middle cerebral artery occlusion (MCAO) for 2 h. Three sets of experiments were conducted to

Role of cardiac work in regulating myocardial biochemical characteristics.

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The purpose of this study was to determine the extent to which functional demand regulates the biochemical character and enzyme capacities of the rat myocardium. Hearts from donor rats were heterotopically transplanted onto the abdominal aorta and inferior vena cava of isogenic recipients. The

Determinants of VO2max in rats after high-intensity sprint training.

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The hemodynamic response to maximal exercise was determined in rats that were subjected to high-intensity sprint training (HIST) and rats that served as sedentary controls. Training consisted of five 1-min bouts of treadmill running at work loads (15% grade, 97 m/min) in excess of the animals'

[Physiology of muscular exercise in children].

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When compared to adults, muscle mass in children is lower and the relative development of aerobic and anaerobic pathways is different. The main consequences are the following: 1) The aerobic metabolism, evaluated by measurement of maximal oxygen uptake (VO2max), is either the same as in adults or

Potential therapeutic applications of fructose-1,6-diphosphate.

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Ischaemia-related tissue injury is the leading cause of death in developed countries. Drugs that can reduce ischaemic injury would be beneficial in treatment of myocardial infarction (MI), surgical trauma and stroke. Fructose-1,6-diphosphate (FDP) is a key intermediate in anaerobic glycolysis and is

Naftidrofuryl oxalate improves impaired brain glucose metabolism after microsphere-induced cerebral embolism in rats.

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The present study was designed to elucidate possible therapeutic effects of naftidrofuryl on the brain glucose metabolism after cerebral ischemia. Cerebral ischemia was induced by injecting 680 microspheres with a diameter of 48 microns into the right internal carotid artery of the rat. After

Uremic myopathy limits aerobic capacity in hemodialysis patients.

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Eleven end-stage renal disease patients trained by stationary cycling during their hemodialysis treatments. After a 6-week control period, 12 weeks of training began and was increased to 30 to 60 minutes at > or = 70% of peak heart rate. Baseline, pretraining and, posttraining exercise tests were

Cerebral metabolism after forced or voluntary physical exercise.

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The pathophysiology of stroke, a leading cause of morbidity and mortality, is still in the process of being understood. Pre-ischemic exercise has been known to be beneficial in reducing the severity of stroke-induced brain injury in animal models. Forced exercise with a stressful component, rather

Preischemic exercise reduces brain damage by ameliorating metabolic disorder in ischemia/reperfusion injury.

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Physical exercise preconditioning is known to ameliorate stroke-induced injury. In addition to several other mechanisms, the beneficial effect of preischemic exercise following stroke is due to an upregulated capacity to maintain energy supplies. Adult male Sprague-Dawley rats were used in exercise

Meclizine-induced enhanced glycolysis is neuroprotective in Parkinson disease cell models.

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Meclizine is a well-tolerated drug routinely used as an anti-histamine agent in the management of disequilibrium. Recently, meclizine has been assessed for its neuroprotective properties in ischemic stroke and Huntington disease models. We found that meclizine protected against

Coordinate induction of energy gene expression in tissues of mitochondrial disease patients.

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We have examined the transcript levels of a variety of oxidative phosphorylation (OXPHOS) and associated bioenergetic genes in tissues of a patient carrying the myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) A3243G mitochondrial DNA (mtDNA) mutation and the skeletal

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