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)

The clinical laboratory furnishes information valuable not only in the diagnosis of myocardial infarction (MI), but also in screening for possible causes of ischemic heart disease through definition of the lipid status of individuals. Accordingly, the panels used in the study of hyperlipidemia as a possible cause of ischemic heart disease are reviewed, including the determination of serum cholesterol, triglycerides, and electrophoretic development of the lipoprotein pattern. The results of an on-going study of more than 500 patients admitted to the emergency room of a general hospital with symptoms of "chest pain" are presented--including the electrocardiogram, enzyme tests, and isoenzyme patterns, in conjuction with the clinical picture. The relative diagnostic value of test procedures is considered, convering the pre-enzymatic period, current test panels, and possible future approaches. It is concluded that the laboratory's position in providing data for diagnosis of MI would be enhanced through development of procedures with as great or greater specificity than the isoenzyme patterns of creatine kinase and lactate dehydrogenase, currently the most specific indicators of MI, but which have results available in two to five minutes.
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PMID:The cardiac profile. 64 63

Analysis of data obtained in the study of the blood enzymatic and isoenzymatic spectra (creatine phosphokinase and lactate dehydrogenase with simulatenous study of aspartate and alanine transaminases) in patients with various forms of ischemic heart disease showed the close correlation of the studied tests with the clinical picture of the disease, the degree and depth of myocardial involvement. The enzymatic tests studied are of diagnostic and prognostic importance and may be used in the differential diagnosis of various forms of ischemic heart disease.
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PMID:[Aspects of a study of the blood enzymatic and isoenzymatic spectrum in different forms of ischemic heart disease]. 67 6

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

The serum creatine kinase (CK), aspartate transaminase (AST), lactic dehydrogenase (LD) and alpha-hydroxybutyric dehydrogenase (HBD) were determined before and 3, 6, 18, and 36 hours after cardiac catheterization and angiocardiography in 56 consecutive patients with ischaemic heart disease. Five of these patients whose serum enzyme levels were higher than normal before the procedure were excluded from the study. Forty-one of the remaining 51 patients had left ventriculography and also selective coronary arteriography. In these 41 patients (groups 1 and 2--see below), the mean serum CK levels increased after the procedure to exceed the upper limit of normal at every study interval. The mean serum AST, LD, and HBD levels generally remained within the normal range at all study intervals, though serum AST increased abnormally in 9 of the 41 patients (22%) and serum LD and HBD each increased above the normal limit in 2 of 41 patients (4.9%). In 24 patients (group 1) whose coronary arteriograms showed insignificant coronary narrowing (less than 75%) in any of the three major coronary arteries, the increase in serum CK was significantly higher than in 17 patients (group 2) with greater than 75% narrowings in at least one of the three major coronary arteries. However, the degree of serum CK elevation observed during the postangiographic period was much lower than that in another group of 30 consecutive patients with acute myocardial infarction. In 10 patients (group 3) who had the same procedure as groups 1 and 2 except without the selective coronary arteriography, the serum enzyme levels showed no noticeable increase after the procedure. The difference in postangiographic serum CK elevation between patients with and without selective coronary arteriography and the difference between group 1 (without significant coronory narrowing) and group 2 (with significant narrowing) strongly suggest that the raised serum CK levels represent some form of myocardial damage caused by the coronary arteriography, which, however, is different at least in degree from that of acute myocardial infarction.
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PMID:Significance of serum enzyme changes after cardiac catheterization and selective coronary arteriography. 125 4

With a canine model of myocardial infarction [ligation of the left anterior descending (LAD) coronary artery] and an intracellular stain for lactic dehydrogenase (LDH) to directly measure size of infarction, the influence of 30 mg. per kilogram of methylprednisolone sodium succinate was evaluted. The intravenous administration of a pharmacologic dose of methylprednisolone one, 2, or 3 hours after the onset of myocardial infarction significantly reduced the ultimate extent of myocardial necrosis, with the greatest reduction seen following the injection of the drug one hour after ligation. The left atrial pressure was significantly decreased by corticosteroid administration, whereas the cardiac index and peripheral vascular tone were improved insignificantly. Inconsistent and/or insignificant effects were observed in the systemic and coronary sinus blood gases and in those indices of myocardial metabolism which were determined. The potential impact of these findings on the clinical applicability of methylprednisolone sodium succinate in acute myocardial ischemia is discussed.
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PMID:Temporal factors in the reduction of myocardial infarct volume by methylprednisolone. 127 68

In view of the hypothesis that free radicals induced damage during ischemia and reperfusion is mediated by transition metals, we investigated the effect of the potent metal chelator TPEN (N,N,N'N'-tetrakis(-)[2-pyridylmethyl]-ethylenediamine) on cardiac function after prolonged myocardial ischemia. Isolated working rat hearts were subjected to 12 hours of cold ischemic arrest followed by reperfusion for 1 hour. The study was carried out on five groups (nine hearts in each): (1) St. Thomas' Hospital cardioplegic solution; (2) St. Thomas' Hospital cardioplegic solution with 7.5 mumol/L TPEN; (3) protection conditions as in group 2, but with TPEN administration during preischemic and reperfusion periods; (4) University of Wisconsin solution; and (5) the same conditions as in group 4 with TPEN administration during the preischemic and reperfusion periods. Significant enhancement of hemodynamic recovery was observed in the presence of TPEN throughout the experiment. The recovery of cardiac output was 24% +/- 4% in group 3, as compared to 12% +/- 4% in group 1 (p < 0.01). The postischemic left ventricular pressure recovery was 57% +/- 4% in group 3, as compared to 18% +/- 7% in group 1 (p < 0.005). The hearts in group 5 recovered, reaching 29% +/- 2% of the preischemic cardiac output and at 65% +/- 2% of the left ventricular pressure recovery (p < 0.05 versus group 3). Lactate dehydrogenase was released throughout the reperfusion. TPEN addition to groups 2 and 3 did not significantly reduce lactate dehydrogenase release; however, TPEN in University of Wisconsin solution and throughout the experiment significantly decreased lactate dehydrogenase release.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:TPEN, a transition metal chelator, improves myocardial protection during prolonged ischemia. 142 Feb 48

Bradykinin perfusion (BK 1 x 10(-12) to 1 x 10(-8) mol/l) of isolated working rat hearts with postischemic reperfusion arrhythmias induced a reduction of the incidence as well as duration of ventricular fibrillation, improvement of cardiodynamics via increased left ventricular pressure, contractility, and coronary flow without changes in heart rate. These beneficial effects were accompanied by reduced activities of the cytosolic enzymes lactate dehydrogenase and creatine kinase as well as lactate output. In the myocardial tissue lactate content was reduced and the energy rich phosphates increased compared to saline perfused control hearts. Glycogen stores were also preserved. These beneficial effects of BK were concentration-dependently abolished by perfusion of the B2 kinin receptor antagonist HOE 140 and the nitric oxide (NO) synthase inhibitor NG-nitro-L-arginine (L-NNA). These results suggest that improved cardiac function during and after myocardial ischemia as well as increased energy rich phophates and glycogen stores are mediated by BK and the subsequent release of NO, shifting myocardial metabolism during ischemia and reperfusion to the glucose pathway which leads to changes indicative for cardioprotection.
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PMID:Bradykinin-mediated metabolic effects in isolated perfused rat hearts. 146 41

Restoration of coronary blood flow after myocardial ischemia is always a matter of urgency, but the resulting surgical or drug-induced reperfusion of ischemic tissue is often associated with myocardial functional disturbances and tissue injury. The present study was carried out to select experimental conditions under which optimal effects of antioxidants can be observed on the adverse effects of reperfusion of ischemic myocardium. The release of lactate dehydrogenase (LDH) and changes in hemodynamic parameters were compared in two models of cardiac reperfusion injury in rat isolated hearts. LDH release from electrically-stimulated hearts perfused under constant flow and with initial (5 min) reperfusion in calcium-free buffer was greater than that from hearts perfused under constant pressure in which ischemia was induced by reduced flow. Combined SOD+catalase was a weak inhibitor of LDH release in both models, ascorbic acid being more potent under constant pressure than under constant flow conditions. A longer ischemic period enhanced the inhibitory effect of ascorbate. Contractility and ventricular end-diastolic pressure recovered slowly during perfusion under constant flow and brief calcium removal, but remained unphysiological under constant pressure. SOD+catalase had no effect on hemodynamic parameters. Ascorbic acid exacerbated ischemia+reperfusion-induced changes in contractility, ventricular pressure, heart rate and coronary flow under constant pressure, but facilitated recovery of contractility on reperfusion under constant flow and brief calcium removal. In studies on antioxidants, different experimental conditions appear to be necessary to observe beneficial effects on tissue damage on the one hand and on hemodynamics on the other. Mild to moderate ischemia, with sustained pacemaker activity, appears to be the condition under which antioxidants provide hemodynamic improvement. In isolated rat hearts, biochemical parameters of tissue damage may be misleading for the effects of antioxidants.
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PMID:Experimental conditions determine effects of ascorbic acid on reperfusion injury: comparison of tissue damage with hemodynamic parameters in rat isolated hearts. 146 51

Phospholipase D (PLD) activity was found to be present in the membrane fraction of rat myocardial cells by in vitro assays (36.7 +/- 4.1 nmol/mg protein per h against 1-palmitoyl-2-arachidonoyl- phosphatidylcholine) and demonstrated in intact cells by the specific transphosphatidylation reaction (in the presence of 0.02% ethanol) quantitated using n-[1-14C]butanol (201.16 +/- 7.1 pmol/min per g dry weight in the whole heart). Both methods showed a significant increase in PLD activity (by 62 and 44%, respectively) in hearts subjected to reversible (30 min) global normothermic ischemia followed by reperfusion (30 min). In hearts prelabeled with [1-14C]arachidonic acid, ischemia/reperfusion induced a significant increase in the amount of radiolabel incorporated into phosphatidic acid (PtdOH) (by 49.6%) and diacylglycerol (DG) (by 259%). DG kinase inhibition by 100 microM dioctanoylethylene glycol did not affect the ischemia/reperfusion DG and PtdOH levels while PtdOH phosphohydrolase inhibition with 40 microM propranolol produced a further increase in PtdOH (to 2.36-fold the baseline level) and a reduction in DG (to only 145% over the baseline levels). Put together, all these results suggest an activation of PLD during myocardial ischemia/reperfusion generating intracellular PtdOH, part of which is converted by PtdOH phosphohydrolase to DG. We further investigated the possible pathophysiological significance of the observed PLD activation. Stimulation of PLD with sodium oleate (20 microM) induced a significant improvement of functional recovery of ischemic hearts during reperfusion (as monitored by coronary flow and left intraventricular pressure measurements) and an attenuation of cellular injury as expressed by lactate dehydrogenase and creatine kinase release in the coronary effluent during reperfusion. These results suggest a PLD-mediated signaling in the ischemic heart which may benefit functional recovery during reperfusion.
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PMID:Phospholipase D signaling in ischemic heart. 161 Sep 13

Local inhibition of angiotensin-converting enzyme (ACE, kininase II) produces both attenuation of angiotensin (Ang) II generation and bradykinin (BK) degradation. To delineate the participation of BK in the cardioprotective actions of ACE inhibitors, experiments were performed in rats and dogs with cardiac ischemia-reperfusion injuries. (I) In rat isolated perfused working hearts with regional myocardial ischemia, BK in concentrations as low as 1 X 10(-9) M increased coronary flow (CF) and reduced the incidence and duration of reperfusion ventricular fibrillation (VF). In addition, enzyme activities of lactate dehydrogenase (LDH) and creatine kinase as well as lactate output were decreased in the venous effluent of BK-perfused hearts, which also showed improved cardiodynamic and metabolic parameters. Even concentrations of BK lower than 1 X 10(-10) M, which were without influence on coronary flow, exerted comparable beneficial metabolic effects connected with reduced incidence and duration of VF. Combined perfusions with threshold concentrations of BK (1 X 10(-12) M) and the ACE inhibitor ramiprilat (2.58 X 10(-9) M), which were ineffective given alone, resulted in a marked cardioprotective effect. Perfusion with Ang II (1 X 10(-9) M) aggravated reperfusion arrhythmias and worsened myocardial metabolism. BK perfusion prevented this deterioration in a concentration-dependent manner, whereas the Ang II receptor antagonist saralasin was only marginally effective. The BK antagonist D-Arg-[Hyp2, Thi5,8, D-Phe7]-BK (1 X 10(-5) M) completely abolished the cardioprotective effects of BK or the ACE inhibitor. However, higher concentrations of BK (1 X 10(-7) M) or ramiprilat (2.58 X 10(-5) M) competitively reversed these properties of the BK antagonist. (II) In anesthetized dogs, BK was infused into the coronary artery in a dose of 1 ng/kg/min during occlusion (90 min) and reperfusion (30 min) of the left descending coronary artery (LAD)--a dose without effects on cardiovascular parameters. In line with the findings in isolated ischemic rat hearts, BK infusion reduced LDH activities and lactate concentrations in the coronary sinus blood, whereas myocardial tissue levels of glycogen and energy-rich phosphates were increased in the infarcted area. The cardioprotective effects produced by perfusion with BK or by reduction of BK degradation through local interference with ACE favor a role for BK in ischemia-reperfusion injuries in rats and dogs.
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PMID:Local inhibition of bradykinin degradation in ischemic hearts. 169 70


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