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)

This study was designed to determine whether human hearts release adenosine, a possible regulator of coronary flow, during temporary myocardial ischemia and, if so, to examine the mechanisms involved. Release of adenosine from canine hearts had been reported during reactive hyperemia following brief coronary occlusion, and we initially confirmed this observation in six dogs hearts. Angina was then produced in 15 patients with anginal syndrome and severe coronary atherosclerosis by rapid atrial pacing during diagnostic studies. In 13 of these patients, adenosine appeared in coronary sinus blood, at a mean level of 40 nmol/100 ml blood (SE = +/-9). In 11 of these 13, adenosine was not detectable in control or recovery samples; when measured, there was concomitant production of lactate and minimal leakage of K(+), but no significant release of creatine phosphokinase, lactic acid dehydrogenase, creatine, or Na(+). THERE WAS NO DETECTABLE RELEASE OF ADENOSINE BY HEARTS DURING PACING OR EXERCISE IN THREE CONTROL GROUPS OF PATIENTS: nine with anginal syndrome and severe coronary atherosclerosis who did not develop angina or produce lactate during rapid pacing, five with normal coronaries and no myocardial disease, and three with normal coronaries but with left ventricular failure. The results indicate that human hearts release significant amounts of adenosine during severe regional myocardial ischemia and anaerobic metabolism. Adenosine release might provide a useful supplementary index of the early effects of ischemia on myocardial metabolism, and might influence regional coronary flow during or after angina pectoris.
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PMID:Release of adenosine from human hearts during angina induced by rapid atrial pacing. 482 35

Human myocardium with focal myocytolysis (vacuolar degeneration, colliquative myocytolysis) was examined by routine light microscopy and by immunoperoxidase staining techniques for creatine kinase (CK) M and B, myoglobin, lactate dehydrogenase (H4)(LDH-1), and aspartate aminotransferase (AST, GOT). Sections of myocardium were selected from autopsy and surgical specimens from patients with and without clinical morphologic evidence of ischemic heart disease. Areas of coagulation necrosis showed loss of enzyme staining, while both normal and myocytolytic cells stained darkly. These results indicate that fibers with myocytolysis retain enzymes and other proteins, indicating sarcolemmal integrity, which is not present in fibers with coagulation necrosis. The implication of these findings is that fibers with myocytolysis are viable; thus, myocytolysis may be a reversible form of myocardial alteration that does not necessarily lead to cell death and eventual myocardial fibrosis.
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PMID:Myocytolysis (vacuolar degeneration) of myocardium: immunohistochemical evidence of viability. 620 21

Experiments were made on 187 white rats weighing 180-200 g. Acute myocardial ischemia was simulated in 137 animals. Fifty sham-operated rats served as control. Experimental acute myocardial ischemia was accompanied by an increase in blood creatine phosphokinase and lactate dehydrogenase activity as well as by an elevation of serum lactate level and fall of blood plasma calcium concentration, suppression of diuresis and excretion of calcium with urine. Intraperitoneal injections of parathyroidine to rats with acute myocardial ischemia led to rapid normalization of the homeostatic parameters. Lethality of experimental animals decreased 1.8-fold.
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PMID:[Effect of parathyroidin on the course of acute myocardial ischemia in experiments on rats]. 662 21

We examined sera from 159 patients with ischemic heart disease and hypertension and from 50 apparently healthy control subjects for content of trace elements, cholesterol, triglyceride, and enzymes. Concentrations of copper, cobalt, cholesterol, and triglyceride were increased in all patients, but calcium was decreased in patients with hypertension, acute myocardial ischemia, and acute myocardial infarction. Also accompanying acute myocardial infarction were decreased concentrations of zinc and iron but increases in nickel, aspartate aminotransferase, alanine aminotransferase, and lactate dehydrogenase. Magnesium concentration was lower in patients with acute myocardial ischemia. In acute myocardial infarction, the concentrations of copper, zinc, and iron were higher after 21-30 h (as compared with the values at 0-10 h), by which time concentrations of calcium, magnesium, cobalt, and alanine aminotransferase had decreased. The variation in concentration of trace elements in serum from cases of ischemic heart disease and hypertension corresponds to the severity of the disorder.
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PMID:Trace elements in serum from Pakistani patients with acute and chronic ischemic heart disease and hypertension. 671 25

The fractions of lipoproteids, lactate dehydrogenase (LDH), malate dehydrogenase (MDH) and their isoenzymes as well as the fructoso-1-phosphate aldolase (F-1-PhA) and cholinesterase (ChE) activity were studied in 220 patients with diabetes mellitus, of which 156 had diabetes mellitus combined with ischemic heart disease (IHD). It was shown that the level of atherogenic lipoproteids is augmented in all the forms of diabetes mellitus and its latent stage, their highest content being seen in the disease, aggravated by IHD. An elevated level of pre-beta-lipoproteid atherogenic fraction was more common in diabetics with IHD. An increased F-1PhA and LDH5 activity was observed in all the patients examined, whereas in severe diabetes mellitus a decrease in the ChE activity was seen. The composed table of changes in the enzyme activity and atherogenic lipoproteid levels in diabetes mellitus combined with IHD, significantly differing from those of the diabetics without IHD, can be used for early IHD diagnosing in diabetes mellitus patients.
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PMID:[Diagnostic coefficients of ischemic heart disease in diabetes mellitus]. 688 7

We immunochemically measured lactate dehydrogenase isoenzyme 1 (LD-1), calculated LD-1/LD ratios (% LD-1) for 122 specimens from 60 patients, and compared the results with those for the conventional cardiac profile and other findings such as clinical presentation and electrocardiogram. Results for LD-1 and % LD-1 could be classified into three groups: group I, with LD-1 less than 64 U/L; group II, with LD-1 greater than 64 U/L and % LD-1 between 17 and 37%; and group III, with LD-1 greater than 64 U/L and 5 LD-1 greater than 38%. These three groups correlated closely and consistently with three patients of cardiac profile, i.e., those of no acute myocardial infarct, myocardial ischemia, and acute myocardial infarct, respectively.
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PMID:Clinical evaluation of immunochemical assay of lactate dehydrogenase isoenzyme 1 in early detection of acute myocardial infarction. 712 46

During the induction of myocardial infarction in the rat by isoproterenol, a decrease in the voltage of the T wave in the electrocardiogram is produced, which reflects myocardial ischemia through a previous infusion of a KCl solution; while the perfusion of NaCl increases the voltage of such wave and therefore cardiac ischemia. The values of free Pi in the myocardium increase significantly with the administration of isoproterenol. If KCl has been perfused previously, the figures of free Pi are superior in 155% of those obtained with the perfusion of NaCl. The values of all the energetic phosphates, AMP, ADP and ATP decrease inversely and in a significant way with isoproterenol and the perfusion of NaCl and KCl. The activity of creatine-phosphokinase in the myocardium decreases with isoproterenol, specially with the previous perfusion of KCl Similarly, the activity of the isoenzimes of lactic dehydrogenase L1 and L2 (alpha-HBDH), decreases, which intensifies with previous perfusion of NaCl, but diminishes with KCl. The activity of malicodehydrogenase (MDH) in the myocardium decreases with isoproterenol, even with the previous perfusion of NaCl, but in lesser degree than with KCl.
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PMID:[Effect of sodium and potassium on cardiac infarct in rats]. 721 55

An in vitro model to study myocardial cell injury was developed with primary monolayer cultures of rat myocardial cells. Two important conditions associated with myocardial ischemia were simulated by depriving the cultures of oxygen and glucose for a specified period of time. Cellular injury caused by hypoxia and glucose deprivation resulted in significant leakage of lactate dehydrogenase (LDH) from the cells into the culture medium. The cells were not lethally injured by treatments as reflected by a lack of change in cell viability and protein content when compared to controls. Pretreatment of cultures with methylprednisolone for 24 hr provided protection to the cells when challenged by hypoxia and glucose deprivation. Methylprednisolone exhibited a dose-response effect in reducing LDH leakage in cultures, which were subsequently deprived of oxygen and glucose for 4 hr. Similar pretreatment with hydrocortisone had no effect in limiting cellular injury in hypoxic and glucose-deprived cultures.
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PMID:Reduction of cell injury in hypoxic cultures of rat myocardial cells by methylprednisolone. 736 54

Serotonin (5-HT) may play a role in exacerbating thrombosis and coronary spasm during myocardial ischemia, but its role in mediating myocardial damage directly is not clear. We determined the effect of the 5-HT2 receptor antagonists cinanserin (0.1-10 microM), ketanserin (0.3-10 microM), and LY 53857 (1-10 microM) on time to contracture, recovery of contractile function, and lactate dehydrogenase (LDH) release after 25-min global ischemia and 30-min reperfusion in isolated rat heart. All 5-HT2 antagonists significantly increased time to contracture in a concentration-dependent manner (EC25 = 1.6, 5.5, and 6.1 microM for cinanserin, ketanserin, and LY 53857, respectively). These compounds also significantly reduced LDH release and improved recovery of contractile function during reperfusion. 5-HT > or = 30 microM significantly reduced time to contracture, indicating a proischemic effect. The proischemic effect of 5-HT was abolished by ketanserin and cinanserin. Inhibition of 5-HT synthesis by parachlorophenylalanine resulted in significant cardioprotection, further indicating the involvement of 5-HT in the pathogenesis of ischemia in this model. Although cinanserin and ketanserin had alpha 1-adrenoceptor blocking effects, LY 53857 was devoid of this activity at concentrations exhibiting cardioprotection. Therefore, 5-HT may exacerbate ischemic injury in rat heart, and this exacerbation appears to be mediated specifically by 5-HT2 receptors.
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PMID:Protective effect of serotonin (5-HT2) receptor antagonists in ischemic rat hearts. 750 71

Nowadays in many European heart centers the activation of the fibrinolytic system, always occurring during cardiopulmonary bypass, is routinely reduced by high-dose application of the proteinase inhibitor aprotinin (total of > 4 million KIU). In this study parameters of myocardial ischemic injury were investigated with the aim of identifying further benefits of aprotinin, particularly the protection of the myocardium during the ischemic period of aortic crossclamping. Forty patients with coronary artery disease who underwent aorta-coronary bypass grafting were randomly and in a double-blind fashion divided into two groups, one that received high-dose aprotinin therapy and one that received only saline solution. Markers such as troponin T, with high specificity for detection of myocardial ischemia and infarction, and markers with more general specificity such as creatine kinase, its isoenzyme, and lactate dehydrogenase showed significantly increased values after ischemia in both groups. In patients who received high-dose aprotinin therapy 3 days after cardiopulmonary bypass all parameters measured showed significantly lower levels compared with those in the control group. Therefore we can presume that the application of high-dose aprotinin provides myocardial protection from perioperative ischemic injury.
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PMID:Lower cardiac troponin T levels in patients undergoing cardiopulmonary bypass and receiving high-dose aprotinin therapy indicate reduction of perioperative myocardial damage. 753 74


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