Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.6.1.3 (ATPase)
 65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Reperfusion injury in early myocardial ischemia was studied in the dog with special reference to sarcoplasmic reticulum (SR) and contraction bands. Acute myocardial ischemia (I) was induced by occlusion of the left anterior descending coronary artery (LAD) for 10, 20 and 30 min followed by reperfusion for 15 min (R). Ca(++)-ATPase activity of SR in 10-min-R-Group was significantly reduced to 60% of control activity, but activity of 10-min-I-Group remained near the control level in subendomyocardium (Endo). ATPase activity in 30-min-I-Group diminished to 60% of control activity in Endo and it was similar for 30-min-R-Group. In ischemic myocardium, composition of major ATPase protein decreased significantly in 30-min-I-Group and similar reduction was observed in 20-min-R-Group in Endo. In morphology proportion of appearance of contraction bands in Endo was significantly increased in 20-min or longer-R-Groups. These results suggest that reperfusion injury is likely to occur when coronary artery is reflowed after 10 min of ischemia. This may be caused by increased intracellular Ca++ at a very early stage of reperfusion period, and reperfusion injury may be induced due to acceleration in the necrotic process of the membrane system in the myocytes during ischemia.
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PMID:Study on reperfusion injury on sarcoplasmic reticulum in acute myocardial ischemia. 153 89

Acute myocardial ischemia and reperfusion in rats increased glutamic oxalacetic transaminase (GOT), non-esterified fatty acid (FFA), malondialdehyde (MDA) content. Furyl-dihydropyridines I 10 mg.kg-1 decreased the release of GOT, FFA, MDA of ischemic myocardium, and prevent ischemia-reperfusion arrhythmia. Furyl-dihydropyridines I increased Na, K-ATPase activity and N-acethylneuraminic acid (NANA) content of erythrocyte membranes, inhibited Ca-ATPase activity of erythrocyte membranes in rats. The results suggested that the mechanism of protecting the ischemic-reperfused myocardium might be associated with the inhibition of cellular lipid peroxidation and Ca-ATPase activity of cell membranes.
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PMID:[Effects of furyl-dihydropyridines I on lipid peroxides of ischemic myocardium and ATPases activity of erythrocyte membranes in rats]. 166 69

Acute heart ischemia induced by ligation of the left coronary artery is associated with variation in the activity of acetylcholinesterase, Na, K-ATPase and Ca, Mg-ATPase in rat erythrocytes. The maximum pronounced variations in the enzymatic activity and in the membrane capacity of erythroblasts for binding direct turquoise are recorded on the 7th day of the experimental myocardial infarction.
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PMID:[Changes in acetylcholinesterase and ATPase activity and certain structural features of the erythrocyte membrane in experimental myocardial ischemia]. 625 88

Acute myocardial ischemia results in a decrease in developed tension and an increase in resting tension. A breakdown of the excitation-contraction coupling system can explain the behavior of the ischemic muscle at a subcellular level. We have identified a specific defect in the sarcoplasmic reticulum (SR) from the ischemic myocardium; i.e., the uncoupling of calcium transport from ATP hydrolysis. The mediators of this excitation-contraction uncoupling process have not been identified. It is now established that the intracellular pH of the ischemic myocardium is in the range of 6.4 but the role of protons and potential role of free radicals have not been identified. We have hypothesized that protons and free radicals may interact to produce the excitation-contraction uncoupling of the ischemic myocardium. Cardiac SR was isolated from the wall of canine left ventricle and calcium uptake velocity and Ca2+ stimulated-Mg2+ dependent ATPase activity determined. Increasing proton concentration between pH 7.0 and 6.4 significantly reduced calcium uptake rates (pH 7.0 = 0.95 +/- 0.02; 6.4 = 0.50 +/- 0.02 mumoles Ca2+/mg-min; p less than 0.01) with no effect on ATPase activity. Calculated coupling ratios (mumoles Ca2+/mumoles Pi) decreased from 0.87 +/- 0.06 at pH 7.0 to 0.51 +/- 0.05 at pH 6.4. At pH 7.0, the generation of exogenous free radicals from the xanthine-xanthine oxidase system significantly depressed both calcium uptake rates (Control = 0.95 +/- 0.02; X+XO = 0.15 +/- 0.02) and ATPase activity (Control = 1.05 +/- 0.02; X+XO + 0.30 +/- 0.01 mumoles Pi/mg-min; p less than 0.01). The decreases in calcium uptake and in ATPase activity were completely reversible with superoxide dismutase (SOD). At pH 6.4 in the presence of xanthine and xanthine oxidase, there is a further depression of calcium uptake rates (Control = 0.50 +/- 0.02; X+XO = 0.11 +/- 0.01; p less than 0.05) but there is no SOD reversible component. The addition of SOD + 20mM mannitol normalized calcium transport at pH 6.4. The calculated coupling ratio at pH 6.4 in the presence of free radicals was 0.13. In contrast sarcoplasmic reticulum isolated from ischemic myocardium demonstrated a significant depression of calcium uptake rates at pH 7.1 which was further accentuated at pH 6.4. Ca2+-ATPase was significantly depressed at pH 7.1 but there was no accentuation at pH 6.4. It is concluded that no single species of free radical can explain the intracellular excitation-contraction uncoupling of the ischemic myocardium. The system can be explained by the interaction of hydrogen ions and superoxide anions producing both injury to the sarcoplasmic reticulum and the formation of lipid free radicals with hydroxyl-like activity.
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PMID:Mediation of sarcoplasmic reticulum disruption in the ischemic myocardium: proposed mechanism by the interaction of hydrogen ions and oxygen free radicals. 630 8

Acute myocardial ischemia reduces tolerance of the heart to arrhythmogenic actions of digitalis glycosides. Because both ischemia and the glycoside produce profound changes in activity of the autonomic nervous system and because sympathetic discharge or catecholamines enhance toxic actions of the cardiac glycosides, the possibility that alterations in digitalis sensitivity of ischemic heart involve changes in sympathetic nerve activity was examined using alpha-chloralose-anesthetized cats. Left anterior descending coronary artery (LAD) was completely occluded by ligation and, 40 min later, a slow i.v. infusion of digoxin was started at a rate of 1 microgram/kg/min. LAD ligation alone did not produce arrhythmias in that condition, but shortened the time to onset of digoxin-induced arrhythmias and thereby reduced the amount of digoxin required to produce the toxic manifestation. Concomitantly, digoxin concentration in plasma and nonischemic areas of the heart were lower in LAD-ligated cats at the onset of arrhythmias than those in sham-operated cats. Myocardial digoxin content in the ischemic area of the LAD-occluded heart was lower than that in nonischemic areas of the same heart. At the onset of digoxin-induced arrhythmias, Na,K-adenosine triphosphatase activity of ischemic myocardium was significantly higher than that in the nonischemic area, reflecting a lower digoxin occupancy of the glycoside binding sites on the sodium pump. Spinal cord (C1) transection or propranolol treatment prolonged the time to arrhythmias in both control and LAD-ligated cats, but failed to abolish the effect of LAD ligation to augment digoxin toxicity. Bilateral vagotomy also did not alter the enhancement of digoxin toxicity caused by ligation of LAD.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of sympathetic nervous system in ischemia-induced reduction of digoxin tolerance in anesthetized cats. 632 71