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)

Protective effects of a perfluorooctylbromide emulsion on myocardial ischemia and reperfusion (MI/R) injury were evaluated in a modified Langendorff rat heart preparation. Isolated rat hearts were equilibrated in Krebs-Henseleit solution (KH) for 35 minutes and perfused with either cardioplegic solution (CPS) or a 100% perfluorooctylbromide (PFOB) emulsion in CPS for 3 minutes. Hearts were then bathed in the emulsion or CPS. Both groups were subjected to 30 minutes of ischemia. Following 30 minutes of ischemia and 30 minutes of reperfusion with KH solution, hearts subjected to the 100% PFOB emulsion showed improved recovery of left ventricular function. Tissue activities of the antioxidant enzymes glutathione peroxidase, superoxide dismutase, and catalase were not affected by the emulsion in this model. Activity of lactate dehydrogenase (LDH) in the bathing medium was elevated at the end of the experimental period in both control and PFOB-treated hearts. The PFOB emulsion reduced the decline in ATP and GSH levels produced by cardioplegia and subsequent reperfusion. No differences were noted in oxidized glutathione (GSSG) levels. These data suggest that the PFOB emulsion provides some protection for the myocardium against injury associated with cardioplegia.
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PMID:Effects of a 100% perfluorooctylbromide emulsion on ischemia/reperfusion injury following cardioplegia. 758 37

We hypothesized that the slowly inactivating component of Na+ current, which is an integral part of the Na+ window current, is a major pathway for Na+ loading during myocardial ischemia. The putative protective effects of tetrodotoxin (TTX) and R-56865, at concentrations that selectively blocked the Na+ window current, as assessed by action potential plateau shortening without affecting maximum upstroke velocity (Vmax), were examined in isolated Langendorff-perfused guinea pig hearts subjected to 50 min of normothermic global ischemia and 60 min of reperfusion. In papillary muscles, TTX reduced action potential duration at > or = 10 nM but reduced Vmax only at > or = 1 microM. R-56865 (10 nM-10 microM) failed to affect Vmax but concentration dependently reduced action potential duration. Ischemia-induced cardiac dysfunction, including increases in left ventricular end-diastolic pressure and lactate dehydrogenase and creatine phosphokinase release at reperfusion, was attenuated by TTX and R-56865 (0.1-320 nM). Ischemic contracture (increase in left ventricular end-diastolic pressure) was abolished by drug concentrations as low as 1 nM, whereas higher concentrations (> 10 nM) of TTX and R-56865 were required to restore systolic function at reperfusion. TTX and R-56865 had little or no effect on hemodynamic variables. Evidence is provided of pronounced and direct cardioprotective effects of low concentrations of R-56865 and TTX in cardiac muscle during ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Alleviation of contractile dysfunction in ischemic hearts by slowly inactivating Na+ current blockers. 765 17

Adenosine released by ischemic myocardial cells stimulates coronary artery vasodilation. Measurement of adenosine concentrations in pericardial fluid in animal models of myocardial ischemia has been used to study the process of adenosine release. To determine whether pericardial fluid adenosine concentrations are increased in human ischemic heart disease, adenosine concentrations were measured in pericardial fluid in 23 subjects undergoing open-heart surgery for coronary artery disease. The results were compared with adenosine concentrations measured in pericardial fluid obtained from 20 subjects undergoing surgery for valvular heart disease. Adenosine concentrations also were measured in pleural fluid obtained during internal mammary artery bypass grafting. Adenosine concentrations were significantly increased in subjects with coronary artery disease compared with fluid obtained from subjects with valvular heart disease (2.47 +/- 0.24 vs 1.36 +/- 0.21 [SEM] microM [p = 0.0013]). Adenosine concentrations were higher in pleural fluid than pericardial fluid from the same individuals. Adenosine concentrations were significantly correlated with pericardial fluid cell counts and lactate dehydrogenase concentrations (r = 0.48; p = 0.0012 and r = 0.77, p = 0.0001, respectively). The results are consistent with myocardial release of adenosine in ischemic heart disease. If adenosine concentrations in pericardial fluid approximate those in myocardial interstitial fluid, sufficient adenosine is present to stimulate adenosine receptor activation in coronary artery smooth muscle.
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PMID:Pericardial fluid adenosine in ischemic and valvular heart disease. 784 59

Effect of myocardial ischaemia on the bioantioxidants levels in the cat heart was evaluated. In addition, effect of curcumin, an anti-inflammatory and anti-thrombotic drug, and quinidine, a standard antiarrhythmic drug, was also studied in the cat. Myocardial ischaemia was induced by the ligation of left descending coronary artery. Quinidine (1 mg/kg, iv) was administered 15 min prior to while curcumin (100 mg/kg, ip) was given 30 min before ligation. Hearts were removed 4 h post coronary artery ligation. Levels of glutathione (GSH), malonaldelhyde (MDA), myeloperoxidase (MPO), superoxide dismutase (SOD), catalase (CAT) and lactate dehydrogenase (LDH) were estimated in the ischaemic and non-ischaemic zones. Both the drugs protected the animals against decrease in the heart rate and blood pressure following ischaemia. In the ischaemic zone, after 4 h of ligation, an increase in the level of MDA and activities of MPO and SOD (cytosolic fraction) were observed. Quinidine and curcumin pretreatment prevented the ischaemia-induced elevation in MDA contents and LDH release. Curcumin pretreatment did not prevent the increase in MPO activity while quinidine did. Results obtained indicate alterations in the bioantioxidants following ischaemia and both curcumin and quinidine prevented ischaemia induced changes in the cat heart.
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PMID:Prevention of ischaemia-induced biochemical changes by curcumin & quinidine in the cat heart. 788 81

We explored the effect of glucose-free hypoxia/reoxygenation of cultured neonatal rat ventricular myocytes on endothelin-1 and alpha 1-adrenoceptor induced activity of the phosphoinositide cycle. At the same time the influence of these agonists on depletion of energy-rich phosphates and cellular damage was assessed. Glucose-free hypoxia did not lead to an increase in basal phospholipase C activity. However, endothelin-1 (10(-8) M) and phenylephrine (10(-5) M) evoked activation of phospholipase C was attenuated after 60 min of hypoxia and declined to 38% and 30% respectively of normoxic values after 90 min of hypoxia. During glucose-free hypoxia, phosphatidylinositol 4,5-bisphosphate, the substrate for phospholipase C, but not phosphatidylinositol or phosphatidylinositol 4-monophosphate was seen to decline to 59% of normoxic values which was independent of activation of phospholipase C by agonists. ATP levels decreased after 30 min of hypoxia and declined to 29% relative to normoxic control after 90 min of hypoxia. Total adenine nucleotide levels showed a similar pattern. The presence of 10(-8) M endothelin-1 during hypoxia did not influence the magnitude of ATP depletion. However, after 15 min of reoxygenation, by itself not significantly leading to recovery of ATP levels, ATP levels were decreased by endothelin-1 as compared to hypoxia/reoxygenation without phospholipase C agonist. Cellular damage as determined by lactate dehydrogenase leakage was not observed during 90 min hypoxia. Reoxygenation resulted in a three-fold increase in enzyme release relative to normoxic control. In the presence of endothelin-1 or phenylephrine this reoxygenation-induced damage was respectively 1.7 and 3.0-fold increased. We conclude that the agonist-induced activity of the phosphoinositide cycle is decreased in time during glucose-free hypoxia, partially through a decrease in phosphatidylinositol 4,5-bisphosphate level. However, the remaining activity may give rise to increased cellular damage. As endothelin-1 and alpha 1-adrenergic amines are known to be released during myocardial ischemia, stimulation of the phosphoinositide cycle by these agonists might be an important factor in determining the magnitude of myocardial injury.
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PMID:Endothelin-1 and phenylephrine-induced activation of the phosphoinositide cycle increases cell injury of cultured cardiomyocytes exposed to hypoxia/reoxygenation. 789 74

1. The effects of beraprost sodium (beraprost) on myocardial infarct size in an anesthetized open-chest canine model of regional myocardial ischemia and reperfusion were investigated. 2. Administration of beraprost (300 ng/kg/min, intravenously) to dogs 45 min after left circumflex coronary artery occlusion until 105 min after reperfusion resulted in a significant reduction in infarct size. 3. The values of control and beraprost treated infarct size expressed as a percentage of the total left ventricle were 15 +/- 3% and 4 +/- 2%, respectively. 4. Reperfusion arrhythmia, plasma creatine phosphokinase (CK) and lactate dehydrogenase (LDH) level were significantly suppressed by treatment with beraprost. 5. By histological examination, beraprost proved to reduce neutrophil migration in the ischemic myocardium after 5 h reperfusion. 6. Therefore, it is suggested that the cytoprotective effect of beraprost during myocardial ischemia and reperfusion may be the consequence of the inhibition of neutrophil migration.
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PMID:Beraprost sodium protects occlusion/reperfusion injury in the dog by inhibition of neutrophil migration. 792 86

It is known that reperfusion of the ischemic myocardium may intensify damage and increase the extent of myocardial necrosis. Oxygen free radicals and their metabolites have been implicated as possible elements in myocardial ischemia-reperfusion injury. In this study in cyanotic patients undergoing open heart operation for tetralogy of Fallot, the myocardial tissue activities of catalase, superoxide dismutase, glutathione peroxidase, and lactate dehydrogenase were determined together with the tissue contents of malondialdehyde, oxidized glutathione, and total glutathione using the spectrophotometric assay method. The tissue activities of catalase, superoxide dismutase, and glutathione peroxidase increased significantly after myocardial reperfusion (p < 0.05) when compared with the tissue activities of the control group (myocardial tissue taken immediately after aortic cross-clamping). The tissue content of malondialdehyde increased significantly after reperfusion (p < 0.05), but the tissue activity of lactate dehydrogenase and the ratio of oxidized glutathione to total glutathione showed an insignificant difference after reperfusion. These data suggest that peroxidation of the cardiac lipids was triggered by the reperfusion of the hypoxic heart, but the myocardial cellular damage was not significant enough to decrease the myocardial lactate dehydrogenase and total glutathione levels. These results also suggest that oxygen free radicals may play an important role in in-vivo myocardial reperfusion stress, but endogenous self-defensive enzyme systems to protect the cell against the cytotoxic oxygen metabolites also were triggered, and the resulting myocardial cellular damage was insignificant.
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PMID:Changes in the antioxidative defensive system during open heart operations in humans. 803 18

The diagnostic significance of ischemia-sensitive laboratory parameters in respect to possible interference with shed blood autotransfusion was assessed in a prospective study with 100 patients undergoing elective coronary artery bypass grafting. Serum levels of creatine kinase, creatine kinase MB activity, creatine kinase MB mass concentration, 2-hydroxybutyrate dehydrogenase, lactate dehydrogenase-1, troponin-T, myoglobin, and glutamicoxaloacetic transaminase were repeatedly assessed up to the sixth postoperative day. Thirty-seven patients were excluded from the study due to postoperative development of myocardial infarction (n = 4), transient ischemic events (n = 25), and left bundle-branch blocks (n = 8). In the remaining group of 63, 37 patients were retransfused with 580 +/- 370 mL shed blood up to the twelfth postoperative hour, and 26 patients did not receive autotransfusion due to minimal mediastinal blood loss. The results of our study show that the ischemia-sensitive laboratory parameters were significantly influenced by shed blood autotransfusion: 8 hours postoperatively, creatine kinase (272%), creatine kinase MB fraction (151%), 2-hydroxybutyrate dehydrogenase (130%), lactate dehydrogenase-1 (133%), troponin-T (200%), myoglobin (159%) and glutamic-oxaloacetic transaminase levels (153%) were significantly elevated (p < 0.05) in patients with postoperative autotransfusion, although there were no electrocardiographic signs of myocardial ischemia in this group of patients. Our study shows that postoperative autotransfusion of mediastinal shed blood may interfere with the diagnosis of perioperative myocardial ischemia by laboratory parameters in coronary bypass patients.
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PMID:Shed blood autotransfusion influences ischemia-sensitive laboratory parameters after coronary operations. 817 1

Dietary copper deficiency affects a number of enzymes, the function of which may influence the outcome of myocardial ischemia-reperfusion injury. Male weanling rats were fed diets that were adequate (> 5 mg/kg) or deficient (< 1 mg/kg) in copper. After 4 wk, the rats' hearts were isolated and used to study the effects of ischemia-reperfusion on intraventricular developed pressure (DevP), positive and negative rates of intraventricular pressure change (+dp/dt and -dp/dt) and release of lactate dehydrogenase and creatine kinase from the heart. The ischemia-perfusion protocol included a 15-min equilibration period, 30 min of warm, total ischemia and reperfusion for 30 min. Preischemic hearts from copper-deficient rats produced lower DevP than hearts from copper-adequate rats at all levels of preload. However, postischemic recovery of DevP was significantly greater in the hearts of the copper-deficient group. Furthermore, the postischemic patterns of lactate dehydrogenase and creatine kinase release in the two groups were significantly different. These findings indicate that, although dietary copper deficiency adversely affects a number of enzymatic systems, the functional recovery of hearts subjected to ischemia-reperfusion injury is improved when the diet is restricted in copper.
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PMID:Isolated hearts from copper-deficient rats exhibit improved postischemic contractile performance. 822 93

It has been hypothesized that intracellular magnesium deficiency is a pathogenetic factor in acute myocardial infarction. This study examined the time course of changes in the erythrocyte magnesium concentration and the correlation between the erythrocyte magnesium concentration and the severity of acute myocardial infarction in 49 consecutive patients with transmural acute myocardial infarction. The data were compared with results from 20 control patients without ischemic heart disease. The erythrocyte magnesium concentration (mg/dl) decreased significantly during the acute phase of the infarction (4.86 +/- 0.09 on day 1, 4.89 +/- 0.10 on day 2 and 4.86 +/- 0.10 on day 3 versus 5.26 +/- 0.19 for controls, all P < 0.05) and then normalized gradually to 5.25 +/- 0.10 on day 28. The serum magnesium concentration (mg/dl) also decreased significantly during the acute phase of the infarction (1.93 +/- 0.04 on day 1 and 2.11 +/- 0.03 on day 2 versus 2.26 +/- 0.08 for controls, all P < 0.05), before recovering to 2.28 +/- 0.06 on day 28. There were significant correlations between the erythrocyte magnesium concentration on day 1 and maximal values of serum cardiac enzymes (r = -0.30 for creatine kinase, r = -0.34 for glutamic oxaloacetic transaminase and r = -0.57 for lactate dehydrogenase, all P < 0.05). Moreover, the erythrocyte magnesium concentration was significantly lower in patients with (4.32 +/- 0.08 mg/dl, n = 13) than in those without (5.06 +/- 0.09 mg/dl, n = 36, P < 0.0001) serious arrhythmias. These data indicate that intracellular magnesium deficiency is involved in the acute phase of myocardial infarction.
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PMID:Intracellular magnesium deficiency in acute myocardial infarction. 824 46


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