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)

We investigated the influence of the thromboxane (TX) synthetase inhibitor HOE 944 (6-(5-Methylimidazol-1-yl)methyl-2-naphthoic acid-Hydrochloride), prostacyclin (PGI2) and indomethacin on reperfusion arrhythmias in isolated perfused ischemic rat hearts. HOE 944, PGI2 and indomethacin were perfused in a concentration of 1 x 10(-6), 5 x 10(-8) and 1 x 10 (-6) mol/l respectively (in vitro). In another set up rats were pretreated p.o. with a daily dose of 30 mg/kg for 7 days (ex vivo). Acute regional myocardial ischemia was induced in isolated working rat hearts by occlusion of the left coronary artery. Reperfusion commenced upon release of this occlusion which was invariably associated with ventricular fibrillations (VF). Perfusion with 1 x 10(-6) mol/l HOE 944 did not affect these arrhythmias. In contrast hearts from HOE 944 pretreated rats were protected against fibrillations (p less than 0.01). PGI2 perfusion was also protective against VF (p less than 0.01) whereas indomethacin perfusion aggravated VF. In the ischemic period cardiodynamics like left ventricular pressure (LVP), dp/dt max and coronary flow (CF) were improved in HOE 944 pretreated rat hearts. In the venous effluent the enzyme activities of lactate dehydrogenase (LDH) and creatine kinase (CK) as well as lactate production were decreased in the ischemic and reperfusion period. Myocardial tissue levels of ATP were distinctly increased and lactate levels decreased in HOE 944 pretreated rats, whereas glycogen and creatine phosphate did not change.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of the thromboxane synthetase inhibitor HOE 944, prostacyclin and indomethacin on reperfusion arrhythmias, cardiodynamics and metabolism in isolated ischemic rat hearts. 307 62

We kinetically measured total lactate dehydrogenase (LD, EC 1.1.1.27), total creatine kinase (CK, EC 2.7.3.2), and aspartate aminotransferase (AST, EC 2.6.1.1.) in 16 elite college basketball players, before the competition season and not in close temporal relation to near-maximal exercise, and in 17 healthy non-athlete controls. LD isoenzymes were determined by both electrophoretic and immunoprecipitation methods. CK-MB isoenzyme was measured electrophoretically. We found significantly higher mean LD-1 values and LD-1/LD-2 ratios in the players than the controls: 31.6 (SD 3.7)% vs 25.8 (SD 3.2)% (P less than 0.005) and 1.1 (SD 0.13) vs 0.87 (SD 0.16) (P less than 0.001), respectively. A "flipped" LD pattern (LD-1 greater than LD-2) was found in half the players and in six of the eight black athletes, but in only two of the control group and in none of the black controls. Mean CK activity in serum exceeded normal values in the serum of the athletes and was higher in comparison with the control group [274 (SD 156) vs 103 (SD 82) U/L]. Mean CK was significantly higher in the eight athletes with the flipped LD pattern than in those with LD-1 less than LD-2 [322 (SD 163) vs 180 (SD 98) U/L; P = 0.05], and also in comparison with CK in the two controls with flipped LD pattern. We saw no significant difference in mean CK between the nine players with normal immunochemical LD-1/LD ratios and the seven players with above-normal ratios. CK-MB was not detected in either athletes or controls. None of the players had any clinical or electrocardiographic evidence for myocardial ischemia or infarction. Evidently the flipped LD pattern usually found in patients with acute myocardial infarction and reported in some athletes after extreme exercise such as ultra-marathon running may also be found in athletes who are in their "basal fitness shape" but who are not involved in competitive physical activity.
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PMID:"Flipped" patterns of lactate dehydrogenase isoenzymes in serum of elite college basketball players. 318 Apr 33

Eight patients with severe peripheral vascular atherosclerosis scheduled for abdominal aortic surgery were investigated to detect coexisting coronary artery disease. None of the patients had a history of angina pectoris or previous myocardial infarction. Preoperative computerised thallium-201 dipyridamole myocardial scintigraphy was abnormal in all patients, showing either myocardial scar tissue and/or ischaemia with redistribution and/or low washout. In all but one patient, the serum level of creatin kinase was elevated during the first postoperative days. In two patients, the serum concentrations of aspartate aminotransferase and lactate dehydrogenase were elevated. None of the patients showed clinical or electrocardiographical signs of acute myocardial infarction. Thallium-201 dipyridamole myocardial imaging is a new noninvasive method for detection of ischaemic heart disease in patients with severe peripheral atherosclerosis who are unable to perform a bicycle exercise test. The new programme for determination of regional washout appeared to be very precise and may be especially applicable in the case of low washout values.
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PMID:Thallium-201 myocardial scintigraphy during dipyridamole-induced coronary hyperaemia. First experiences with a new regional washout programme. 321 87

Alterations in cation homeostasis during and after recovery from myocardial ischemia may account for some of the reversible and irreversible components of myocardial cell injury. To investigate possible mechanisms involved, we exposed cultured layers of spontaneously contracting chick embryo ventricular cells to media containing 1 mM cyanide (CN) and 20 mM 2-deoxyglucose (2-DG), and zero glucose for up to 6 h, and then allowed cultured cells to recover in serum-free culture medium for 24 h. Changes in Na, K, and Ca contents, 42K uptake and efflux, ATP content, cell water content, and lactate dehydrogenase (LDH) release were measured, and compared with changes produced by exposure to 10(-3) M ouabain and severe hypoxia. Exposure to CN and 2-DG caused marked increase in cell Na (sevenfold) and Ca (fivefold) contents, and a decrease in K content (one-fifth normal), coincident with ATP depletion to one-tenth normal levels. This produced only slight cell injury, evidenced by increased LDH release. Recovery for 24 h resulted in return to near normal values (expressed in nanomoles per milligram of protein) of Na, Ca, and ATP contents. However, there was failure of cell K content to return to normal, associated with a persistent reduced net uptake of 42K, and an increase in the rate of 42K efflux. These abnormalities in K homeostasis were associated with a decrease in cell volume and water content per milligram of protein. More marked ATP depletion (to 1/100 normal values) was produced by hypoxia plus 2-DG and zero glucose, and was associated with much more severe cell injury manifested by LDH loss. Ouabain exposure resulted in a much greater Ca gain (20-30-fold), relative to increase in Na content, than did either CN and 2-DG or hypoxia; and ouabain effects were not reversible (after a 15-fold or greater increase in Ca content was produced) and were associated with significant LDH release. We conclude that these cells are resistant to cell injury caused by moderately severe Ca overload and ATP depletion produced by exposure to CN and 2-DG. However, metabolic inhibition of ATP production produces persistent abnormalities in K homeostasis, associated with functional abnormalities.
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PMID:Alterations in cation homeostasis in cultured chick ventricular cells during and after recovery from adenosine triphosphate depletion. 335 Sep 67

Oxygen-derived free radicals and intracellular calcium overload have been implicated as mediators of myocardial ischemia/reperfusion injury. We hypothesized that free radical scavengers or calcium channel blockers could enhance the protection afforded the isolated, working rat heart by crystalloid cardioplegia against this type of injury at 37 degrees C. Hearts from 42 male rats in seven groups (n = 6) were studied in an isolated, working heart preparation measuring aortic flow (ml/min/gm dry wt), peak systolic pressure (mm Hg), coronary artery flow (ml/min/gm dry wt), and calculated coronary vascular resistance (dyne.sec.cm-5/gm dry wt). Creatine kinase and lactate dehydrogenase release were measured before ischemia and at various times during the postischemic reperfusion period. Time-matched control hearts (group 1) were perfused for 2 hours. After finding that 30 minutes of ischemia and 10 minutes of reperfusion (group 2) produced significant (p less than 0.01) functional impairment that was completely protected (group 3) by a preischemic bolus of St. Thomas' Hospital cardioplegic solution, we again found significant (p less than 0.01) functional impairment after 40 minutes of ischemia and 10 minutes (group 4) or 20 minutes (group 5) of reperfusion despite a preischemic bolus of St. Thomas' Hospital cardioplegic solution. Diltiazem (10 mg/L) plus St. Thomas' Hospital cardioplegic solution (group 6) did not significantly (p less than 0.01) enhance functional recovery. Addition of superoxide dismutase plus catalase (200 microns/ml) (group 7) produced marked improvement in functional recovery that did not differ significantly (p less than 0.01) from control results (group 1). The creatine kinase and lactate dehydrogenase data strongly supported the preceding functional data. Coronary flow and vascular resistance were not significantly (p less than 0.01) changed from control values in any group. We conclude that the addition of superoxide dismutase and catalase but not diltiazem to St. Thomas' Hospital cardioplegic solution can significantly enhance myocardial protection against normothermic ischemia/reperfusion injury. This implicates oxygen-derived free radicals as mediators of this type of injury.
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PMID:Enhancement of crystalloid cardioplegic protection against global normothermic ischemia by superoxide dismutase plus catalase but not diltiazem in the isolated, working rat heart. 336 28

The following parameters were studied in 27 newly diagnosed and not treated patients with primary hypothyroidism: TTH, creatine kinase (CK) with MB isoenzyme, lactate dehydrogenase (LDH) with isoenzymes LDH1 and LDH5, aspartate aminotransferase (ASAT) and alanine aminotransferase (ALAT) before and after 20-day substitutive therapy. It has been established that the enzymes were increased in about 60% of the untreated patients, and the typical enzyme constellation for hypothyroidism consisted of CK with MB isoenzymes, ASAT and LDH1. The myocardial isoenzymes were normalized within the period of substitutive therapy. The enzymes were established to be elevated only in the patients that had increased CK. The follow up of the above enzyme constellation before and during the initial phases of the treatment of hypothyroidism could provide considerable possibilities of differential diagnosis with ischemic heart disease, often manifested during that period. The determination of CK in advance would be a screening determining the necessity of studies on the enzyme constellation.
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PMID:[Serum enzymes in hypothyroidism]. 360 1

The purpose of the study was to find out the character of the restructuring of enzymes and isoenzymes of creatine kinase (CK), lactate dehydrogenase (LDH) and glucose-6-phosphate-dehydrogenase (G 6 P-DH) in the myocardium, which occurs in patients with ischaemic heart disease (IHD), and to compare the activity of the aforementioned enzymes in the myocardium of patients with IHD, examined intra vitam, and in patients who died suddenly. An analysis was made of 11 samples obtained by myocardial biopsy from the left ventricle of patients with IHD and of 11 samples obtained at autopsy of patients with IHD who have died a sudden death. Serving as controls was bioptic material from the myocardium of 12 patients without IHD. In the myocardium of patients with IHD, examined intra vitam, a decrease in the activity of the mitochondrial isoenzyme CK (MiMi) and the isoenzyme LDH-1, and a considerable rise in the activity of G 6 P-DH were found. In patients with IHD, who have died suddenly, there was found only a decrease in isoenzyme LDH-1 activity and a reduced concentration of CK B-units. The experiments proved that the differences in the myocardial isoenzyme spectrum between the two groups of patients with IHD are not connected with the process of autolysis.
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PMID:Isoenzyme spectrum of creatine kinase and lactate dehydrogenase in the myocardium of patients with ischaemic heart disease. 379 5

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


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