Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151814 (coronary occlusion)
 3,687 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The limitation of a myocardial necrotic area by some energy-yielding compounds in rat coronary occlusion and their capacity to elevate the ischemia threshold in conscious rabbits were studied. Sodium malate, ascorbic acid and phosphoenolpyruvate were demonstrated to reduce the sizes of necrotic areas and increase the ischemia threshold, whereas cytochrome C and fructose-1,6-diphosphate were effective solely in limiting the infection area. It was concluded that the preventive antianginal effect of energy-yielding and electron-accepting compounds depended on their capacity to accumulate in intact cardiomyocytes.
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PMID:[A comparative evaluation of the cardioprotective and antianginal actions of energy-providing agents]. 145 76

Influence of fructose++-1,6-diphosphate, succinate, malate and cytochrome C on free lipid peroxidation (FLP), infarct sizes and metabolic acidosis was studied in experiments on rats. The good correlation between inhibition of FLP and cardioprotector activity was established for activators of glycolytic energy production only. Krebs' cycle metabolites limited the zone of myocardial necrosis after coronary occlusion without any significant depression of FLP. Succinate and malate were practically inactive under acute metabolic acidosis of isolated rat heart.
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PMID:[Relationship of antioxidant and anti-ischemic effects of various energy-yielding compounds]. 166 19

Myocardial oxygenation may be altered markedly by changes in tissue blood flow. During brief ischemia and reperfusion produced by transient occlusion of the left anterior descending artery in 10 open-chest dogs, changes in the oxygenation of tissue hemoglobin (Hb) plus myoglobin (Mb) and the oxidation-reduction (redox) state of mitochondrial cytochrome aa3 were monitored continuously using near-infrared spectroscopy. The nondestructive optical technique indicated that coronary occlusion produced an abrupt drop in tissue oxygen stores (tHb02 + Mb02), tissue blood volume (tBV), and the oxidation level of cytochrome aa3. Changes in the cytochrome oxidation state were related inversely to transmural collateral blood flow within the ischemic region (r = 0.77) measured with radiolabeled microspheres. Furthermore, there was a direct relationship (r = 0.91) between collateral blood flow and the tissue level of desaturated Hb and Mb (tHb + Mb). Reperfusion after 2 min of ischemia led to a synchronous overshoot of baseline in coronary flow and tBV followed by supranormal increases in tHb + Mb02 and the oxidation level of cytochrome aa3. The tHb + Mb level increased transiently during reperfusion. This response correlated inversely with collateral flow during ischemia (r = 0.91). Accordingly, the time required to reach peak tHb + Mb levels was shortest in dogs with high collateral flows (r = 0.75). Thus collateral blood flow partially sustains myocardial oxygenation during coronary artery occlusion and influences tissue reoxygenation early during reperfusion.
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PMID:Dynamic mechanisms of cardiac oxygenation during brief ischemia and reperfusion. 217 24

Infarct size varies in untreated animals subjected to coronary artery occlusion at the same anatomic site. The relation between the hypoperfused zone and the magnitude of myocardial salvage when different pharmacologic interventions are used remains to be established. Thus, in 95 anesthetized dogs, 1 minute after left anterior descending coronary occlusion, technetium-99m-labeled albumin microspheres (8 mCi) were injected into left atrium for the assessment of the hypoperfused zone. Fifteen minutes after coronary occlusion 42 dogs were randomized into a control group and 53 into a treated group. In the treated group, 6 dogs received nifedipine, 0.35 micrograms/kg followed by 2.4 micrograms/kg/hour; 7 received diltiazem, 0.2 mg/kg followed by 0.9 mg/kg/hour; 13 received bepridil, 2.5 mg/kg; 9 received cytochrome C, 2.5 mg/kg; 8 received rutosides, 200 mg/kg; and 10 received nifedipine plus cytochrome C. All drugs were administered intravenously. At 6 hours the dogs were killed and their hearts were cut into 3-mm-thick slices. Infarct size was determined by triphenyltetrazolium chloride staining; the hypoperfused zone was delineated by autoradiography. The dogs were retrospectively subgrouped as follows: those with small hypoperfused zones, i.e., less than 15% of the left ventricle (controls n = 8, treated n = 7) and those with large hypoperfused zones, i.e., more than 15% of the left ventricle (controls n = 34, treated n = 46). In dogs with large hypoperfused zones, treatment salvaged 42 +/- 3% of the myocardium destined to undergo necrosis, whereas in those with small hypoperfused zones 78 +/- 10% of myocardium was salvaged (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relation of myocardial salvage to size of myocardium at risk in dogs. 407 32

It has been shown that a single intravenous injection of obsidan (0.1 mg/kg) to dogs during acute coronary occlusion results in a decrease in the activities of "a" phosphorylase, Mg-dependent ATPase, creatine phosphokinase, succinate dehydrogenase and cytochrome-c-oxidase, in a slight lowering of the ATP content accompanied by the increased content of AMP and unchanged concentration of creatine phosphate. Repeated injections of the drug in the same dose raise the activities of the enzymes up to the control level and produce activation of glycogenolysis and succinate dehydrogenase during the reparative period. The drug favours the preservation of "b" phosphorylase activity in the infarcted tissue and does not change the content of adenine nucleotides and creatine phosphate upon prolonged application.
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PMID:[Effect of prolonged beta-adrenergic blockade on myocardial energy metabolism in coronary occlusion]. 712 83

In contrast to traditional therapy (beta-adrenoblocker and nitrates), energostim improves the systolic and diastolic functions of myocardium during 120-min occlusion of the left descending coronary artery. The energostim-induced improvement in the central hemodynamics is correlated with an adaptive increase in activity of the antioxidant system enzymes in response to the ischemic production of reactive oxygen species, which is evidence of the mobilization of reserves of the enzymatic link in the antioxidant defense system of cardiomyocytes. Analogous pattern is observed in the blood. In the control group of traditional therapy, a decrease in the superoxide dismutase (SOD) activity and the redox potential (NAD/NADH) in myocardium are correlated with a decrease in the maximum rate of pressure increase in the left ventricle (R 6.4, p < 0.01) observed 2 h after the coronary occlusion. In the energostim treated group, there is a correlation between the SOD activity and the content of cytochrome C in mitochondria (R 6.1, p < 0.01): a change in the level of cytochrome C during 2-h acute ischemia is correlated with the decrease in redox potential (NAD/NADH) and in the ratio of glutathione peroxidase to Mn-dependent SOD (r 0.64, p < 0.01). Thus, disturbances in the antioxidant defense system of both myocardium and blood plasma of the patients with acute myocardium infarction are correlated with inability of the energy supply system to utilize oxygen in the process of glycolysis and oxidative phosphorylation in mitochondria. Stable adaptive increase in activity of the antioxidant defense system enzymes and a decrease in the content of cytochrome C in the blood plasma are probably the independent indications of beneficial prognosis and high efficacy of the proposed treatment of the ischemic damage of myocardium.
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PMID:[Effect of energostim on myocardial damage during coronary artery occlusion]. 1465 Feb 8