cytochrome oxidase/infarction

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Changes in enzyme activity (glutamic oxaloacetic transaminase, lactic dehydrogenase, cytochrome c, and cytochrome oxidase) in serum and heart muscle after experimental myocardial infarction in the dog.

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Experimental renal infarction. I. Changes in succinic dehydrogenase and cytochrome oxidases activity.

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Expression of the peptide hormone hepcidin increases in cardiomyocytes under myocarditis and myocardial infarction.

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The micronutrient iron is an essential component that plays a role in many crucial metabolic reactions. The peptide hormone hepcidin is thought to play a central role in iron homeostasis and its expression is induced by iron overloading and inflammation. Recently, hepcidin has been reported to be

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

Aluminum Phosphide Poisoning Presenting like Acute Myocardial Infarction in a Young Girl.

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Aluminium phosphide poisoning is very common in India. It is one of the most fatal poisons. The clinical spectrum of poisoning varies depending upon the dosage and duration of consumption. The main effect of the poison is due to the release of phosphine which inhibits cytochrome oxidase and thereby

Myocardial cytochrome oxidase activity is decreased following carbon monoxide exposure.

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Carbon monoxide (CO) inhalation often leads to cardiac dysfunction, dysrhythmias, ischemia, infarction, and death. However, the underlying mechanism of CO toxicity is poorly understood. We hypothesize that inhaled CO interrupts myocardial oxidative phosphorylation by decreasing the activity of

Myocardial infarction sensitizes medial prefrontal cortex to inhibitory effect of locus coeruleus stimulation in rats.

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Anxiety is a common comorbidity that develops after myocardial infarction and is now an established independent risk factor for cardiovascular mortality. Here, we assessed anxiety and mapped neural activity of forebrain regions that regulate anxiety in a rat model of myocardial infarction in order

Some myocardial factors of biological oxidation in experimental myocardial infarction.

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In 175 dogs myocardial infarction was produced by high ligation of descending branch of left coronary artery. At various intervals after the intervention (1, 3, 5, 10, 30, 180 days), the activities and levels of NAD, NADH, FAD, riboflavin, cytochrome C, myoglobin, some NAD-dependent Krebs cycle

[Myocardial infarction secondary to carbon monoxide poisoning--a study of two cases].

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The carbon monoxide poisoning still remains a main cause of fatal poisoning. The carbon monoxide poisoning occurs after inhalation of carbon monoxide. Carbon monoxide binds strongly to molecules, such as cytochrome oxidase, myoglobin, hemoglobin, causing hypoxia of tissues and organs. Carbon

Brain oxymetry in the operating room: current status and future directions with particular regard to cytochrome oxidase.

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Near-infrared spectroscopy (NIRS) is a cerebral monitoring method that noninvasively and continuously measures cerebral hemoglobin oxygenation and the redox state of cytochrome oxidase using highly tissue-permeable near-infrared light. This technique now has wide clinical application, and its

No evidence for reduced thrombocyte cytochrome oxidase activity in Alzheimer's disease.

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We measured cytochrome oxidase activity in thrombocytes from patients with senile dementia of the Alzheimer type. We found no decrease in enzyme activity in Alzheimer's disease patients when compared with patients with multi-infarct dementia, with young control donors, and with age-matched control

[Metabolic shifts in acute period of myocardial infarct and the possibility of their correction with curantil].

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The effect of curantil on the values of energy metabolism in different parts of the myocardium was studied on dogs with experimental myocardial infarction. Tissue respiration, the activity of Krebs' cycle enzymes, cytochrome oxidase, pentose phosphate cycle and glycolysis, and the content of

Delayed ischemic preconditioning activates nuclear-encoded electron-transfer-chain gene expression in parallel with enhanced postanoxic mitochondrial respiratory recovery.

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BACKGROUND Delayed ischemic preconditioning promotes cardioprotection via genomic reprogramming. We hypothesize that molecular regulation of mitochondrial energetics is integral to this cardioprotective program. RESULTS Preconditioning was induced by use of 3 episodes of 3-minute coronary artery

Characterization of autoantigenic sites on isolated dog heart mitochondria.

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1. Anti-heart mitochondria autoantibodies were developed in serum from dogs following experimental myocardial infarction. 2. Heart mitochondria frozen and thawed repeatedly in a sucrose/Tris-chloride buffer retained both their functional integrity as measured by the respiratory control ratio and

[The structuro-functional state of the ischemic myocardium under the action of a terrilitin-nicotinic acid mixture in animal experiments].

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Histochemical evidence of the activity and distribution of glycolysis redox enzymes, tissue respiration and terminal oxidation pattern (dehydrogenase of lactic, malic, succinic and isocitric acids, NAD-N- and NADPh-N-ase, cytochrome oxidase) as well as the levels of the major carbohydrates

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