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[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

[Free ribonucleotides and the activity of enzymes of the pentose phosphate cycle in cardiac muscle in experimental myocardial infarct].

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[Enzyme activity in post-infarct aneurysm and in the myocardial zone outside the infarct in experimental infarct in rats].

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Activities of lactate dehydrogenase, glucose-6-phosphate dehydrogenase, transketolase and creatine phosphokinase were studied in tissue of aneurysm and in extrainfarctional part of rat heart muscle after experimental infarction. Activity of total LDH, content of its anode isoenzymes and creatine

[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

Metabonomic study of Chinese medicine Shuanglong formula as an effective treatment for myocardial infarction in rats.

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A UPLC/TOF-MS-based metabonomic study was conducted to assess the holistic efficacy of Traditional Chinese Medicine Shuanglong Formula (SLF) for myocardial infarction in rats. Thirty male Sprague-Dawley rats were randomly divided into five groups after surgery. The Panax ginseng group, Salvia

Regulation of and intervention into the oxidative pentose phosphate pathway and adenine nucleotide metabolism in the heart.

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The capacity of the oxidative pentose pathway (PPP) in the heart is limited, since the activity of glucose-6-phosphate dehydrogenase (G-6-PD), the first and regulating enzyme of this pathway, is very low. Two mechanisms are involved in the regulation of this pathway. Under normal conditions, G-6-PD

Pentose phosphate pathway activation via HSP27 phosphorylation by ATM kinase: A putative endogenous antioxidant defense mechanism during cerebral ischemia-reperfusion.

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Molecular mechanism underlying ischemic stroke remains poorly understood. We previously reported glucose 6-phosphate dehydrogenase (G6PD) activity in pentose phosphate pathway (PPP) is activated via heat shock protein 27 (HSP27) phosphorylation at serine 85 (S85) by ataxia telangiectasia mutated

Metabolite profiling of blood from individuals undergoing planned myocardial infarction reveals early markers of myocardial injury.

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Emerging metabolomic tools have created the opportunity to establish metabolic signatures of myocardial injury. We applied a mass spectrometry-based metabolite profiling platform to 36 patients undergoing alcohol septal ablation treatment for hypertrophic obstructive cardiomyopathy, a human model of

Reduced Nicotinamide Adenine Dinucleotide Phosphate, a Pentose Phosphate Pathway Product, Might Be a Novel Drug Candidate for Ischemic Stroke.

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OBJECTIVE Our previous study has defined a role of TP53-induced glycolysis and apoptosis regulator in neuroprotection against ischemic injury through increasing the flow of pentose phosphate pathway. We hypothesized that the pentose phosphate pathway product nicotinamide adenine dinucleotide

[The effect of alpha-ketoglutarate, malate and alpha-glycerophosphate on bioenergetic processes in ischemic myocardium].

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Anti-ischemic action of exogenous natural metabolites and their effect on biological combustion processes indexes in cardiac muscle has been investigated on white rats with the experimental myocardial infarction. It has been established that the marked cardioprotective effect of malate and

Endogenous level of TIGAR in brain is associated with vulnerability of neurons to ischemic injury.

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In previous studies, we showed that TP53-induced glycolysis and apoptosis regulator (TIGAR) protects neurons against ischemic brain injury. In the present study, we investigated the developmental changes of TIGAR level in mouse brain and the correlation of TIGAR expression with the vulnerability of

[Enzyme activity in the normal atrioventricular node and in the bundle of His in young children].

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The authors examined by histochemical methods the atrioventricular node and the bundle of His in five infants who died from unnatural deaths and in a four-and-half-year-old child who died immediately following haemorrhagic infarction of the gut. Both structures differed, similarly as in adult age,

Glutathione and K(+) channel remodeling in postinfarction rat heart.

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Electrical remodeling of the diseased ventricle is characterized by downregulation of K(+) channels that control action potential repolarization. Recent studies suggest that this shift in electrophysiological phenotype involves oxidative stress and changes in intracellular glutathione (GSH), a key

[Metabolic changes in blood cells in various forms of ischemic heart disease].

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In various clinical types of heart ischemic disease (stenocardia of stress and rest, large scale- and small scale myocardial infarction) alterations in activity of glycolysis and Krebs cycle enzymes as measured in leukocytes were especially distinct under conditions of large scale myocardial

Aerobic glycolysis fuels platelet activation: small-molecule modulators of platelet metabolism as anti-thrombotic agents.

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Platelets are critical to arterial thrombosis that underlies myocardial infarction and stroke. Activated platelets, regardless of nature of stimulus, initiate energy-intensive processes that sustain thrombus, while adapting to potential adversities of hypoxia and nutrient deprivation within the

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