Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In Langendorff-perfused rat hearts, the perfusion pressure was reduced from 100 cm H2O to 20 cm H2O for 30 minutes to produce a model of global ischemia with a residual oxygen uptake. The release of lactate dehydrogenase (LDH) and the occurrence of ventricular arrhythmias during reperfusion were dependent on the substrate. Glucose-perfused hearts had the highest rates of glycolytic ATP production (2.5 mumol/g per min) during ischemia with normal contents of tissue cyclic adenosine 3',5'-monophosphate (cAMP) and, during reperfusion, the release of LDH was lowest and severe ventricular arrhythmias did not occur. In pyruvate-perfused hearts, glycolysis was inhibited during ischemia, the rate of production of glycolytic ATP was only 0.5 mumol/g per min. and tissue cAMP doubled; during reperfusion, LDH release was 14-fold higher and ventricular arrhythmias were more severe. Total tissue contents of ATP and phosphocreatine were similar in glucose- and in pyruvate-perfused hearts. In hearts perfused with acetate, there was virtually no glycolytic ATP synthesized during the last 5 minutes of ischemia and cAMP increased further. Acetate- and palmitate-perfused hearts showed greatest release of LDH and had severest arrhythmias during reperfusion, suggesting that it was the metabolic and not the detergent effects of palmitate that were operating. Lipolysis was not a major factor in the cause of reperfusion LDH release. A role of glycolytic ATP in the maintenance of membrane integrity is postulated.
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PMID:Effects of substrates on tissue metabolic changes in the isolated rat heart during underperfusion and on release of lactate dehydrogenase and arrhythmias during reperfusion. 20 59

To clarify the value of serum enzymes in the detection of intraoperative and postoperative myocardial injury associated with coronary artery bypass grafting, we evaluated 70 consecutive patients (151 grafts). We used electrocardiograms and serial determinations of serum levels: serum glutamic oxaloacetic transaminase (SGOT), creatinine phosphokinase (CPK), lactic dehydrogenase (LDH), and LDH isoenzymes on Days zero, 1, 3, 5, 7, and 10. Patency of all grafts 1 week postoperatively was 92 per cent. Fourteen patients (20 per cent) had ECG evidence of acute myocardial infarction (AMI) or ischemia lasting longer than 48 hours. This incidence of AMI was attendant with no deaths or discernible changes in postoperative ventriculography. LDH-1 (cardiac fraction) was elevated in all patients with myocardial injury. Late elevation of LDH-1 occurred in 2 patients at the time of postoperative catheterization, 1 of whom had negative findings on ECG. Diagnostic correlation was not observed with total LDH, CPK, or SGOT. Predisposing factors to AMI included preinfarction angina (4 of 14 patients), occluded grafts (4 of 14), and a bypass time greater than 120 minutes.
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PMID:Myocardial injury and bypass grafting. Value of serum enzymes in diagnosis. 24 Sep 85

Primary cultures of rat heart endothelial cells were subjected to simulated conditions of ischemia: hyposia and glucose deprivation for 4 and 24 hr. Cellular injury was evaluated by measuring changes in viability, total protein, cellular morphology, and leakage of cytoplasmic enzymes from the cells into the culture medium. Deprivation of oxygen and glucose for 4 or 24 hr did not lethally injure the cells as noted by no change in cell viability, morphology, and total protein when compared to controls. However, reversible or non-lethal cellular injury was produced as reflected by a significant release of lactate dehydrogenase (LDH) from the cells into the medium after treatment with hypoxia and glucose deprivation for 4 or 24 hr. When the cultures were deprived of glucose, but were oxygenated, cellular injury was not evident after 24 hr. Deprivation of oxygen but not glucose resulted in significant loss of LDH after 4 or 24 hr. When the cultures were allowed to recover after oxygen and glucose deprivation in complete medium containing 1000 mg glucose per 1 and a normal atmosphere of 20% O2, they had levels of LDH leakage comparable to those of control cultures.
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PMID:Injury to primary cultures of rat heart endothelial cells by hypoxia and glucose deprivation. 54 Sep 18

Creatine kinase (CK), lactic dehydrogenase (LDH), and more recently their isoenzyme determinations (CK-MB and LDH1) have been useful adjuncts in verification of myocardial injury. To determine whether DC cardioversion affects these serum enzyme levels, we recorded total CK, total LDH, CK-MB, and LDH1 levels serially during 24 hours following elective DC cardioversion in 18 patients without cardiac ischemia. New postcardioversion elevations in total CK and total LDH levels were small and occasional: CK (one of 18 patients), LDH (four of 18 patients). Elevations of CK-MB or LDH1 following cardioversion did not develop in any of the patients. Therefore, new CK-MB or LDH1 elevations associated with arrhythmias must result from myocardial damage to DC cardioversion.
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PMID:Direct current cardioversion. Effect on creatine kinase, lactic dehydrogenase and myocardial isoenzymes. 57 71

An in vitro model of myocardial ischemia has been established with primary monolayer cultures of postnatal rat myocardial cells. Ischemic conditions were simulated in vitro by subjecting the myocardial cell cultures to various levels of oxygen and glucose deprivation. The experimental protocol consisted of treatment with 20% or 0% O2 and 1000, 500 or 0 mg glucose per 1 of medium for 4 or 24 hr. Control cultures were treated with 20% O2 and 1000 mg glucose. After the ischemic treatments, cultures of beating muscle (M) cells were evaluated for signs of injury, i.e. leakage of cytoplasmic enzymes into the culture medium. Differences were found in leakage of lactate dehydrogenase (LDH) and creatine phosphokinase (CPK) from the cultures that were exposed to partial ischemia of glucose deprivation and from those cultures that were exposed to total ischemia of oxygen and glucose deprivation. Glucose deprivation along resulted in a slight-to-moderate loss of LDH and CPK from the cells, whereas total ischemia resulted in a significant release of the two cytoplasmic enzymes. When the cultures were allowed to recover after ischemic treatment in complete medium (1000 mg glucose) and a normal atmosphere of 20% O2, they had levels of LDH leakage comparable to those of control cultures. Cell viability and total protein content of the ischemic cultures did not differ significantly from controls.
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PMID:Ischemic myocardial injury in cultured heart cells: leakage of cytoplasmic enzymes from injured cells. 68 9

It has been proposed that a single preoperative dose of a corticosteroid may protect the myocardium from ischemic injury during open heart surgery. To test this hypothesis, a prospective, randomized, double blind study was carried out in ninety-five patients undergoing coronary bypass surgery using intermittent ischemic arrest with systemic and local hypothermia. Half the patients received 2 gm (approximately 30 mg/kg) of methylprednisolone 2 hours prior to the initiation of cardiopulmonary bypass and the other half received a placebo. Postoperative electrocardiograms and blood levels of serum creatine phosphokinase (CPK), lactic dehydrogenase (LDH), and serum glutamic oxalacetic transaminase (SGOT) were compared in the two groups. No apparent difference was noted in the number of patients with significantly elevated levels of CPK, LDH, or SGOT or in the number with positive isoenzyme patterns of CPK and LDH. Moreover, there was no significant difference in the mean values of CPK, LDH, or SGOT between the two groups. The number of patients with electrocardiographic evidence of myocardial injury (10 per cent) was the same in both groups and no difference was noted in (1) the ease with which patients could be weaned from cardiopulmonary bypass, (2) postoperative arrhythmias, (3) postoperative bleeding, (4) postoperative respiratory insufficiency, and (5) length of hospital stay. It is concluded that a single preoperative dose of 2 gm of methylprednisolone offers no demonstrable protection to the myocardium from the effects of ischemia during coronary artery bypass surgery.
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PMID:Effect of methylprednisolone on myocardial preservation during coronary artery surgery. 77 98

The measurement of lactate dehydrogenase (LDH) release into perfusates after hypothermic storage was found to be a reliable index of ischemic injury of rabbit kidneys. Kidneys were exposed to warm and cold ischemia for varying periods. Each kidney was perfused before and after storage at simple hypothermia with 25 ml of a modified Collins solution. The venous effuent was collected in 5 ml fractions. Total LDH activity was measured in the first fraction after storage and used as a measure of ischemic tissue damage. It was confirmed that increasing the period of cold ischemia result in significant increases in LDH activity. The release of LDH into perfusates was then used to compare kidney damage after preservation with various fluids. With this method, it was not possible to demonstrate any difference in the extent of tissue damage after preservation with sodium-rich vs. potassium-rich perfusion fluid. Addition of steroids, vitamins and essential amino acids did not prevent or reduce tissue damage, estimated in this way. The effects of adding cryoprotectants to the perfusion fluid varied; LDH release following addition of 5% DMSO was significantly greater, and after addition of 5% glycerol smaller than the release after perfusion with a modified Collins solution alone. Stepwise addition of DMSO up to 20% resulted in serious tissue damage with a large LDH release into the perfusate.
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PMID:LDH release into perfusates of preserved kidneys. 78 32

Changes in liver integrity were studied in isolated perfused cat livers during simulated shock conditions (i.e., combined hypoxia, acidosis, and ischemia) or under the influence of each hypodynamic state separately. The combined hypodynamic stimuli depressed carbon clearance 51% and significantly elevated lactic acid dehydrogenase (LDH) and cathepsin D activities in the perfusate. The perfused liver was more seriously affected by hypoxia than by acidosis or ischemia alone. Reticuloendothelial clearance was depressed 20% and 25% in acidosis and hypoxia, respectively. Hypoxia also induced a 3-fold increase in cathepsin D and a 13-fold increase in LDH activities in the perfusate. After 150 min of hypoxia or ischemia, free cathepsin D in liver tissue increased significantly. The impairment of liver cell integrity (i.e., of Kupffer and parenchymal cells) occurred between 60 and 90 min during simulated shock conditions, indicating that the liver is stable for 60 min when it is exposed to hypoperfusion. The perfused liver is sensitive to local stimuli that predominate in circulatory shock, particularly hypoxia. These stimuli promote the release of lysosomal and cytoplasmic enzymes as well as depress phagocytosis by the reticuloendothelial system, phenomena that exacerbate the shock state.
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PMID:Hepatic cell integrity in hypodynamic states. 99 83

In thrombocytes of patients with ischemic and hemorrhagic insult a transformation in the isozyme spectrum of lactate dehydrogenase was observed without an alteration in the reaction rate. In this case LDH3 was decreased and LDH1 and LDH4 were increased. The correlation was not found between the type of insult and the character of the isozyme spectrum. The alterations were considered as an adaptive mechanism and the reflected the extent of immediate or intermediate effect of ischemia on thrombocytes.
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PMID:[Activity of lactate dehydrogenase and its isoenzymes in the thrombocytes in different forms of cerebral circulatory disorder]. 103 Aug 86

The perfused rat heart was used to assess the possible contribution of glycolytically produced ATP to the maintenance of the action potential in the normoxic heart, and to the maintenance of membrane integrity in the underperfused, ischemic heart. During normoxia, pyruvate (10 mM) was nearly as able as glucose (10 mM) to maintain the normal action potential. During ischemia (reduction of perfusion pressure of Langerdorff heart from 100 to 20 cm H2O), total tissue values of ATP and creatine phosphate were similar in pyruvate and in glucose hearts. However, pyruvate-perfused hearts had higher tissue levels of cyclic AMP during the ischemic period, and during the reperfusion period they had an increased release of lactate dehydrogenase and an increased incidence of arrhythmias when compared with glucose hearts. It is proposed that these differences can be related to a higher rate of production of glycolytic ATP. The anatomical, biochemical, and pharmacological evidence favoring a cytoplasmic compartment of ATP located in relation to the cell membrane is reviewed.
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PMID:Glycolytic ATP and its production during ischemia in isolated Langendorff-perfused rat hearts. 103 48


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