Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.6.1.1 (aspartate aminotransferase)
 21,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fifty consecutive patients undergoing coronary artery bypass grafting for chronic stable angina were assessed by serial electrocardiography, preoperative and postoperative myocardial scanning with technetium-99m pyrophosphate, gated radionuclide ventriculography, and serial measurement of creatine kinase, aspartate aminotransferase, urea stable lactic dehydrogenase, and creatine kinase isoenzyme (MB) to assess the incidence of perioperative myocardial infarction and identify the most appropriate diagnostic techniques. The correlation between myocardial scanning and the measurement of peak enzyme and isoenzyme activity was excellent in the diagnosis of perioperative infarction, although electrocardiography proved less helpful. There appeared to be no advantage in measuring creatine kinase MB rather than the more routinely measured enzymes. There were two deaths and evidence of myocardial infarction in five other patients, an incidence of 14%. Perioperative infarction was associated with a significant reduction in resting ejection fraction in two cases. In those patients without evidence of perioperative infarction the mean increase in ejection fraction of 7.8% was statistically significant.
 ...
PMID:Myocardial infarction related to coronary artery bypass graft surgery. 632 26

We utilized immunoperoxidase methods to study the distribution of both cytosolic or soluble(s) and mitochondrial (m) aspartate aminotransferase (AspAT) in normal, ischemic, and necrotic myocardium. Human myocardium was obtained from autopsy (n = 9) and surgery (n = 6). Cardiac tissue from 26 dogs with experimental myocardial infarction induced by closed-chest balloon occlusion and four dogs with myocardial ischemia without necrosis induced by a 50% reduction in left main coronary artery flow for 3 hours were studied. Duration of occlusion was 45 minutes (n = 1), 3 hours (n = 11), 5 to 6 hours (n = 10), or 15 to 24 hours (n = 4). Highly purified m- and s-AspAT and specific antibodies were prepared in our laboratory. In all cases, control experiments were performed. Microscopically normal human and dog myocardium uniformly stained for m- and s-AspAT. Necrotic myocardium from patients with infarcts showed markedly reduced immunostaining. In those dogs with myocardial necrosis, all dogs with coronary occlusion of 5 to 24 hours, and eight of 11 dogs with 3-hour occlusions, immunostaining was significantly reduced for both s- and m-AspAT in regions confirmed to be necrotic by triphenyl tetrazolium chloride and hematoxylin and eosin staining. Myocardial necrosis was confirmed in the 3-hour infarcts by electron microscopy. In the four dogs with a 50% reduction in left main flow for 3 hours, and one dog with a 45-minute coronary occlusion, ischemia was demonstrated by glycogen loss in period acid-Schiff-stained sections but there was no evidence of necrosis by electron microscopy or triphenyl tetrazolium chloride staining and there was no loss of immunostaining evident for s- or m-AspAT. Thus, s- and m-AspAT were visualized in normal and ischemic myocardium with decreased staining in necrotic tissue using immunoperoxidase techniques. Loss of both s- and m-AspAT can be demonstrated in human myocardium and in experimental canine myocardium as early as 3 hours after coronary occlusion and appears to be specific for irreversible myocardial injury. No depletion of isoenzyme can be detected by immunohistochemical techniques in tissue that is ischemic but not necrotic. Furthermore, by these immunoperoxidase techniques, loss of s- and m-AspAT from necrotic myocardium appears to be simultaneous.
 ...
PMID:Distribution of cytosolic and mitochondrial aspartate aminotransferase in normal, ischemic, and necrotic myocardium. An immunohistochemical study. 638 75

Aminotransferases are ubiquitous enzymes of mammalian cells and several are of important diagnostic use. The application of aspartate aminotransferase activity measurements in serum from individuals suffering from myocardial infarction brought about a new dimension in clinical laboratory testing in the 1950s. This review focuses on measurement techniques for aspartate aminotransferase and their application (a subsequent article will review other aminotransferases). Assay techniques measuring enzyme activity are direct spectrophotometric measurements, manometric techniques, assays using dye substances, coupled enzyme techniques, and radiometric procedures. Of these procedures, the one employing malate dehydrogenase and NADH is the most important and is covered in particular detail. The estimation of the mitochondrial isoenzyme of aspartate aminotransferase is also of clinical interest, in particular for estimating severity of disease or in specific applications (e.g., chronic alcoholism). Methods reviewed for estimation of this enzyme are electrophoresis, chromatography, differential kinetic behavior, and immunochemical separation. Determination of the enzyme protein by techniques independent of its catalytic activity are also reviewed.
 ...
PMID:Measurement of aminotransferases: Part 1. Aspartate aminotransferase. 639 17

The mechanism of the protein leak from exercised muscle remains obscure, but may be related to depletion of intracellular high-energy phosphate and/or to mechanical disruption. The high levels of creatine kinase (CK) and other muscle proteins found in plasma for several days after marathon running, especially downhill running, are due to protein efflux from skeletal muscle. There is no evidence that marathon running damages the healthy, well-perfused myocardium, despite the fact that the plasma levels of total creatine kinase (CK), the isoenzyme CK-MB, CK-MB/total CK (%), myoglobin, aspartate transaminase, lactate dehydrogenase and tropomyosin may be the same as after myocardial infarction. These indices must be interpreted with the greatest caution when found in anyone who habitually undertakes strenuous exercise, especially if they have done so within the previous week.
 ...
PMID:Plasma creatine kinase after the marathon--a diagnostic dilemma. 652 95

The relationship between histologically determined infarct size and release or peak levels of circulating cardiac enzymes and myosin light chain 2 (LC2) was studied. Myocardial infarction was produced by ligating the left anterior descending coronary artery in 18 conscious closed-chest dogs. Creatine phosphokinase (CPK), cytosolic and mitochondrial isozymes of aspartate transaminase (sAST and mAST) in the plasma, and LC2 in the serum were measured serially until 10 days after infarction, when infarct size was determined histologically [range 4.0-38.8% of the left ventricular weight (%LV)]. Infarct size correlated most closely with LC2 release (r = 0.82, P less than 0.001) and less closely with peak sAST (r = 0.59, P less than 0.01), peak mAST (r = 0.49, P less than 0.05), peak CPK (r = 0.22), and CPK release (r = 0.14). The correlation between infarct size and CPK release was improved by limiting the analysis to the dogs with infarct size of less than 20% LV (n = 11, r = 0.53, P less than 0.1). Because, among cardiac enzymes and LC2, CPK activity decayed most rapidly in the lymph fluid when incubated in vitro, degeneration of CPK in the lymph stream may contribute to the nonlinear relationship between infarct size and CPK release.
 ...
PMID:Evaluation of methods for estimating infarct size by myosin LC2: comparison with cardiac enzymes. 661 89

An examination of 400 coronary patients demonstrated a relationship between increased serum CPK, AST, LDH and LDH-1, and the spread and severity of myocardial infarction (MI). In transmural and large-focal MI, CPK activity peak observed on Day 1-2 of the disease was increased 4-12-fold, and that of AST, 5-fold, as compared to the upper limit of the normal range. In small-focal and subendocardial MIs, the increase was 1.5-8-fold and 3-fold, respectively. In angina pectoris, serum CPK activity also showed an increase, although a less manifest one. A CPK activity level of 175 IU is proposed as a discriminative level to be used in the diagnosis of large-focal myocardial infarctions.
 ...
PMID:[Assessment of the results of serum enzyme studies in different forms of myocardial infarction]. 662 Aug 15

Enzyme kinetics for creatine kinase (CK), CK-MB, aspartate aminotransferase (AST), and lactate dehydrogenase (LD) in serum were followed in 14 patients who had suffered acute myocardial infarction and who were given intracoronary streptokinase shortly (mean 4.9 h, SD 2.6 h) after onset of symptoms. In the 10 patients for whom thrombolysis was successful, CK activity peaked earlier (12.8 vs 21.6 h) and at higher values (3548 vs 2436 U/L) than in the four patients for whom the treatment was unsuccessful. The mean maximum rate of increase in CK was threefold greater in the former group (574 vs 169 U/L per hour), but the total amount of CK released into the circulation and the fractional disappearance rates were similar for both groups. The profiles for AST and CK-MB for successfully treated patients closely resembled those for CK. LD, however, peaked significantly later than CK (25.7 vs 12.8 h). Early peaking of CK or CK-MB after nonsurgical reperfusion can be potentially useful as a noninvasive in vitro index to the success of therapy of myocardial infarction with thrombolytic agents.
 ...
PMID:Activities of some enzymes in serum after therapy with intracoronary streptokinase in acute myocardial infarction. 671 33

Mitochondrial and cytoplasmic isoenzymes of aspartate aminotransferase (AST) were studied in the sera of 42 patients following acute myocardial infarction and compared to creatine kinase (CK), lactate dehydrogenase (LDH) and alanine aminotransferase (ALT). Mitochondrial AST( ASTm ) was detected in 93% (39/42) of patients. Maximum recorded ASTm activity was 59.5 +/- 8.8 U/l and was found 39.4 +/- 3.5 hours after the onset of symptoms (chest pain) of myocardial infarction. In contrast the maximum recorded cytoplasmic AST ( ASTc ) activity was greater (327 +/- 23 U/l) and it occurred earlier (33.5 +/- 2.2 hours) after onset of infarction compared to ASTm . ASTm correlated significantly (p less than 0.05) with ASTc , LDH and ALT but not with total CK or CK-MB. ASTc correlated significantly (p less than 0.05) with total CK, CK-MB and LDH but not ALT. Maximum recorded ASTm activity was significantly associated with the clinical assessment of left ventricular failure ( Killip classification) but not with ventricular arrhythmias. In a subset of 15 patients evaluated with invasive hemodynamic measurements of cardiac output and pulmonary capillary wedge pressure. ASTm correlated significantly (p less than 0.05) and better than CK-MB with the hemodynamic assessment of left ventricular dysfunction. Thus ASTSm can be readily identified in sera of patients after acute myocardial infarction and may be of value in the evaluation of patients with acute myocardial infarction.
 ...
PMID:Mitochondrial and cytoplasmic isoenzymes of aspartate aminotransferase in sera of patients after myocardial infarction. 672 62

Fifty consecutive patients, 25 undergoing aortic valve replacement and 25 mitral valve replacement, were studied by serial electrocardiography, preoperative and postoperative technetium-99m pyrophosphate radionuclide scanning, and serial measurement of enzymes (creatine kinase, aspartate aminotransferase, urea stable lactic dehydrogenase) and the MB isoenzyme of creatine kinase to define the incidence of preoperative myocardial infarction and to identify the most appropriate diagnostic techniques. The use of myocardial scanning and measurement of peak enzyme activity proved to be accurate indicators of myocardial infarction, but the electrocardiogram was of limited value. The measurement of creatine kinase MB isoenzyme had no diagnostic advantage over that of the other enzymes. There were two deaths in the series, one due to acute pancreatitis after aortic valve replacement and the other due to myocardial injury after mitral valve replacement. There were four non-fatal myocardial infarctions after aortic valve replacement, giving an incidence of 16%, and none after mitral valve replacement, giving an incidence of 4%.
 ...
PMID:Myocardial infarction related to valve replacement surgery. 673 91

The possibility of predicting myocardial infarct size from early enzyme measurements was studied using a physiological two compartment distribution model. Based on this the time dependent appearance function in plasma was calculated for creatine kinase, aspartate aminotransferase, and lactate dehydrogenase in 29 patients suffering from acute myocardial infarction. On average, the appearance function of the three enzymes started four hours after the onset of symptoms, and the maximum was reached after 12 hours for creatine kinase, 13 hours for aspartate aminotransferase, and 22 hours for lactate dehydrogenase. The cumulated appearance function was used as an acceptable estimate of infarct size. The prediction of infarct size from defined points of the appearance function curve for each of the three enzymes was attempted according to a set schedule during the first 25 hours after the onset of myocardial infarction. The prediction using creatine kinase was superior to the other enzymes. Even so, a reliable prediction could only be established at the very earliest from nine hours and this is too late, as irreversible loss of myocardium occurs rapidly after the onset of symptoms. This, together with the fact that other models have unacceptable variability of the prediction, lead to the conclusion that enzymatic predictive models are of no practical value in clinical intervention studies to reduce infarct size.
 ...
PMID:Limitation of enzymatic models for predicting myocardial infarct size. 686 May 13


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>