Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Quantitative histochemical assays of several enzymes (succinic, lactic, beta-hydroxybutyrate, alpha-glycerophosphate, and glucose-6-phosphate dehydrogenases, NAD diaphorase, and phosphorylase) in the myocardium of persons who had died suddenly with postinfarctional cardiosclerosis have failed to reveal any changes specific for this patient group. Direct correlations were established between the enzyme activities assayed, on the one hand, and the extent of myocardial hypertrophy and the signs of chronic heart failure, on the other. The activities of beta-hydroxybutyrate dehydrogenase and glucose-6-phosphate dehydrogenase, which are involved in fatty acid utilization and in the pentose phosphate pathway, were elevated in cases of moderate hypertrophy, as were those of all redox enzymes in cases of strongly marked hypertrophy, although they were reduced in cases with signs of chronic cardiac failure despite the presence of considerable myocardial hypertrophy. Areas of acute myocardial ischemia were discovered in 45% of the cases.
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PMID:[Histochemical study of the enzyme activity of the myocardium of sudden death victims with postinfarct cardiosclerosis]. 296 Feb 98

The purpose of the study was to find out the character of the restructuring of enzymes and isoenzymes of creatine kinase (CK), lactate dehydrogenase (LDH) and glucose-6-phosphate-dehydrogenase (G 6 P-DH) in the myocardium, which occurs in patients with ischaemic heart disease (IHD), and to compare the activity of the aforementioned enzymes in the myocardium of patients with IHD, examined intra vitam, and in patients who died suddenly. An analysis was made of 11 samples obtained by myocardial biopsy from the left ventricle of patients with IHD and of 11 samples obtained at autopsy of patients with IHD who have died a sudden death. Serving as controls was bioptic material from the myocardium of 12 patients without IHD. In the myocardium of patients with IHD, examined intra vitam, a decrease in the activity of the mitochondrial isoenzyme CK (MiMi) and the isoenzyme LDH-1, and a considerable rise in the activity of G 6 P-DH were found. In patients with IHD, who have died suddenly, there was found only a decrease in isoenzyme LDH-1 activity and a reduced concentration of CK B-units. The experiments proved that the differences in the myocardial isoenzyme spectrum between the two groups of patients with IHD are not connected with the process of autolysis.
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PMID:Isoenzyme spectrum of creatine kinase and lactate dehydrogenase in the myocardium of patients with ischaemic heart disease. 379 5

Alterations in activities of lactate- and glucose-6-phosphate dehydrogenases and in the LDHisozyme spectra in human heart muscle after sudden death, caused either by acute ethanol intoxication or by ischemic heart disease, were characterized by inhibition of aerobic oxidation and activation of the glycolytic pathway of energy formation.
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PMID:[Glucose-6-phosphate dehydrogenase and lactate dehydrogenase activities and lactate dehydrogenase isoenzyme spectrum in human myocardium after sudden death caused by acute alcohol intoxication and ischemic heart disease]. 688 Jan 24

A moderate reduction in coronary blood flow results in decreased myocardial oxygen consumption, accelerated glycolysis, decreased pyruvate oxidation, and lactate accumulation. To quantitatively understand cardiac metabolism during ischemia, we have developed a mechanistic, mathematical model based on biochemical mass balances and reaction kinetics in cardiac cells. By numerical solution of model equations, computer simulations showed the dynamic responses in glucose, fatty acid, glucose-6-phosphate, glycogen, triglyceride, pyruvate, lactate, acetyl-CoA, and free-CoA as well as CO2, O2, phosphocreatine/creatine, nicotinamide adenine dinucleotide (reduced form)/nicotinamide adenine dinucleotide (oxidized form) (NADH/NAD+), and adenosine diphosphate/adenosine triphosphate (ADP/ATP). When myocardial ischemia was simulated by a 60% reduction in coronary blood flow, the model generated myocardial concentrations, uptakes, and fluxes that were consistent with experimental data from in vivo pig studies. After 60 min of ischemia the concentrations of glycogen, phosphocreatine, and ATP were decreased by 60%, 75%, and 50%, respectively. With the onset of ischemia, myocardial lactate concentration increased and the myocardium switched from net consumer to net producer of lactate. Our model predicted a rapid 13-fold increase in NADH/NAD+, but only a twofold increase in the ratio of acetyl-CoA to free-CoA. These findings are consistent with the concept that pyruvate oxidation is inhibited during ischemia partially by the rise in NADH/NAD+.
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PMID:Mechanistic model of myocardial energy metabolism under normal and ischemic conditions. 1196 72

Exercise provides numerous salutary effects, but our understanding of how these occur is limited. To gain a clearer picture of exercise-induced metabolic responses, we have developed comprehensive plasma metabolite signatures by using mass spectrometry to measure >200 metabolites before and after exercise. We identified plasma indicators of glycogenolysis (glucose-6-phosphate), tricarboxylic acid cycle span 2 expansion (succinate, malate, and fumarate), and lipolysis (glycerol), as well as modulators of insulin sensitivity (niacinamide) and fatty acid oxidation (pantothenic acid). Metabolites that were highly correlated with fitness parameters were found in subjects undergoing acute exercise testing and marathon running and in 302 subjects from a longitudinal cohort study. Exercise-induced increases in glycerol were strongly related to fitness levels in normal individuals and were attenuated in subjects with myocardial ischemia. A combination of metabolites that increased in plasma in response to exercise (glycerol, niacinamide, glucose-6-phosphate, pantothenate, and succinate) up-regulated the expression of nur77, a transcriptional regulator of glucose utilization and lipid metabolism genes in skeletal muscle in vitro. Plasma metabolic profiles obtained during exercise provide signatures of exercise performance and cardiovascular disease susceptibility, in addition to highlighting molecular pathways that may modulate the salutary effects of exercise.
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PMID:Metabolic signatures of exercise in human plasma. 2050 14