Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P17174 (aspartate aminotransferase)
 14,872 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We evaluated the utility of serum enzyme and isoenzyme activities for detecting autopsy-proved perioperative myocardial infarction in patients who died after cardiac operations. We studied 79 patients who had autopsies performed after coronary artery bypass grafting or valve replacement, or both. Thirty-seven had histologic evidence of a perioperative myocardial infarction. We found statistically significant differences between the group of patients with infarction and the group without infarction when we compared the mean activities of creatine kinase, creatine kinase MB, aspartate aminotransferase, and the lactate dehydrogenase-1/lactate dehydrogenase-2 ratio. The postoperative changes in serum enzymes were analyzed by logistic regression for their relation to perioperative myocardial infarction. Creatine kinase MB exhibited the best diagnostic association with the presence of perioperative myocardial infarction. The lactate dehydrogenase-1/lactate dehydrogenase-2 ratio correlated to a lesser extent with infarction. Adjustment of the diagnostic cutoff to 133 U/L for creatine kinase-MB measured 15 hours after operation yielded a sensitivity of 0.60 and a specificity of 1.0. This study demonstrates that no combination of enzyme activity changes after operation can completely discriminate all patients with perioperative myocardial infarction from those without. Nonetheless, measurement of creatine kinase MB activity provide 96% accuracy for diagnosing infarction at a prevalence of 10%.
J Thorac Cardiovasc Surg 1989 Nov
PMID:The predictive value of serum enzymes for perioperative myocardial infarction after cardiac operations. An autopsy study. 281 7

Isolated working hearts of 16 month old spontaneously hypertensive rats (SHR, n = 8) and age matched Wistar-Kyoto (WKY, n = 8) rats were exposed to 30 min global normothermic ischaemia followed by 60 min reperfusion. The hearts were routinely perfused at an afterload level of 13.3 kPa and a preload level of 1.0 kPa. The control values of left ventricular pressure, its maximal positive first derivative (dP1v/dtmax), coronary flow per gram heart tissue, and release of lactate and enzymes such as lactate dehydrogenase and aspartate aminotransferase were comparable in both groups. WKY rat hearts ejected almost twice as much perfusate per gram heart weight as the SHR hearts. In pressure-flow curves, obtained during the control period in SHR hearts, cardiac output was independent of changes in afterload, varying between 10.7 and 18.7 kPa. In contrast, in WKY rat hearts increases in afterload resulted in a progressive decrease in cardiac output. Reperfusion of the SHR hearts after 30 min of global normothermic ischaemia resulted in a poor recovery of cardiac output (13% of the control values) and dP1v/dtmax (32%) compared with the values in the WKY rat hearts (66% and 91% of the control values respectively). Reactive hyperaemia was prominent in the WKY rat hearts but completely absent in the SHR hearts. During one hour reperfusion, SHR hearts lost 3.5 times more lactate dehydrogenase and 2.5 times more aspartate aminotransferase than the WKY rat hearts. Pressure-flow curves, obtained during the reperfusion period, showed modest recovery of myocardial function of the WKY rat hearts at the lowest afterload level tested but completely depressed myocardial function of the SHR hearts at all afterload levels. Heart tissue contents of adenosine triphosphate and creatine phosphate after one hour of reperfusion were lower in the SHR than in the WKY rats, but compared with native values a comparable percentage decrease was seen in both groups of rats.
Cardiovasc Res 1986 Jan
PMID:Myocardial function in normal and spontaneously hypertensive rats during reperfusion after a period of global ischaemia. 293 55

Myocardial activities of several enzymes were measured in infarcted and non-infarcted areas of heart sections obtained from eight patients who died after acute myocardial infarction. Similar data were obtained from four patients with cardiovascular disorders who died from causes other than myocardial infarction and from six patients without previously known heart disease. It was found that both non-infarcted and infarcted tissue samples contained considerably altered enzyme activities. This finding explains the low correlations between enzymatic and histological estimates of infarct size previously reported. However, when the residual myocardial activities of different enzymes were compared with each other, a close correlation was found between creatine kinase, alpha-hydroxybutyrate dehydrogenase, and aspartate aminotransferase. It appears that the pathological changes in the myocardial activities of these enzymes may be explained by the phenomenon of diluted myocardium. This indicates that myocardial injury, as estimated from plasma enzyme activities, may still be expressed meaningfully in gram equivalents of healthy myocardium.
Cardiovasc Res 1988 Sep
PMID:Myocardial enzyme depletion in infarcted human hearts: infarct size and equivalent tissue mass. 324 32

In this study neonatal rat heart cell cultures were evaluated on their potential merit for studying the oxidative component in the cardiotoxic action of drugs. Cumene hydroperoxide was used as a model compound. Cumene hydroperoxide induced enzyme release from the myocyte cultures which appeared to be both dose- and substrate(glucose)-dependent. Significant correlations were found between depletion of GSH and increased GSSG formation on the one hand and enzyme release on the other hand. Furthermore the formation of malondialdehyde, one of the products of lipid peroxidation, was measured, which correlated with enzyme release as well. Measurements on the release of the mitochondrial isoenzyme of aspartate aminotransferase imply that the lipid peroxidative process affects primarily the sarcolemmal membrane. The results indicate that myocytes in culture can provide a convenient in vitro system to assess the peroxidative action of cardiotoxic agents.
Cardiovasc Res 1986 Jan
PMID:Lipid peroxidation in neonatal rat heart cell cultures: effects of cumene hydroperoxide. 370 38

Twenty-three patients underwent cardiac surgery for valve replacement, valve reconstruction, aorto-coronary bypass grafting, aneurysmectomy or combinations of these. Excised cardiac tissue was obtained from left ventricular (LV) papillary muscle (17 patients), LV outflow tract (3 patients), or LV aneurysms (3 patients). A total of 34 myocardial samples, collected from excised cardiac tissue, were analysed for creatine kinase (CK), CK-isoenzymes, cytoplasmic and mitochondrial isoenzymes of aspartate aminotransferase (cAST and mAST, respectively), and lactate dehydrogenase (LDH) isoenzymes. Myocardial CK activity correlated positively with preoperative LV ejection fraction (p less than 0.001), negatively with the preoperatively measured extent of LV wall motion abnormalities (p less than 0.001), and negatively with preoperative LVEDP (p less than 0.02). Myocardial CK activity was negatively correlated with preoperative validity class (p less than 0.005). However, no correlation existed between myocardial CK activity and postoperative validity. Excluding the biopsies from LV aneurysms, myocardial CK activity was positively correlated with the fraction H-subunits in LDH (p = 0.02), and was negatively correlated with the fraction mAST in total AST (p less than 0.005). While cAST activity was proportional to CK activity in the biopsies from VL papillary muscle and LV outflow tract, mAST activity declined only with 2.4 +/- 1.2% per 10% fall of CK. The increase of mAST/cAST ratio with decreasing CK, together with the decrease of LDH-H/LDH and CK-M/CK ratios with decreasing CK, indicated the presence of an adaptation process in a myocardium with low CK activity rather than a process of necrosis.(ABSTRACT TRUNCATED AT 250 WORDS)
Thorac Cardiovasc Surg 1984 Oct
PMID:A comparative study on enzymatic data from myocardial biopsies and cardiac function in patients who underwent cardiac surgery. 608 15

In a prospective study, 93 patients were observed up to nine months after open-heart surgery using hypothermia, hemodilution and cold cardioplegia. In the first two weeks frequent determinations were made of serum aminotransferase, alkaline phosphatases (ALP), lactic dehydrogenase isoenzymes, gamma glutamyltransferase (GT), total and free bilirubin and bile acids. Plasma hemoglobin was measured at the end of the operation. After the first period, aminotransferases, alkaline phosphatases and bilirubin were determined monthly. On the first postoperative day almost all of the patients showed abnormal aspartate aminotransferase (ASAT) activity and ASAT/ALAT (alanine aminotransferase) greater than 1, and about 25% had hyperbilirubinemia. The findings suggested early postoperative leakage of enzymes not only from the myocardium, but also from the liver. After two weeks the patients presented another pattern of liver dysfunction, with abnormal ALAT in 50%, ASAT/ALAT less than 1, and abnormal ALP and GT in 28 and 45%, respectively. Eight patients were judged to have post-transfusion hepatitis of non-A, non-B type. Six of them had abnormal aminotransferases for more than six months.
Scand J Thorac Cardiovasc Surg 1984
PMID:Hepatic dysfunction after open-heart surgery. 615 78

Impairment of contractile function and extent of release of several intracellular marker enzymes and DNA were studied in isolated perfused rat hearts after low-flow (0.16 ml . min-1) ischaemia followed by 2 h of reperfusion and after anoxia followed by 2 h of reoxygenation. After varying periods of ischaemia or anoxia, the hearts were analysed for cytoplasmic, lysosomal and mitochondrial enzymes, for nuclear DNA and for increase in heart weight (oedema formation). Recovery of contractile function, weight increase and release of lactate dehydrogenase (LDH), a cytoplasmic enzyme, were measured as a function of duration of ischaemia or anoxia. Myocardial enzyme activities and DNA content after varying periods of ischaemia or anoxia were compared with myocardial LDH activity. The study demonstrates that the ultimate extent of enzyme depletion after ischaemia + reperfusion differs significantly from that after anoxia + reoxygenation in respect of mitochondrial enzymes. For mitochondrial aspartate aminotransferase and monoamine oxidase ultimate depletion is 64 +/- 8% and 114 +/- 22%, respectively, for hearts after ischaemia + reperfusion, and 7 +/- 8% and 58 +/- 11%, respectively, for hearts after anoxia + reoxygenation. It is concluded that mitochondrial damage, as reflected by mitochondrial enzyme release from the heart, is less marked after anoxia + reoxygenation than after ischaemia + reperfusion at corresponding extent of LDH depletion.
Cardiovasc Res 1984 Dec
PMID:A comparative study on ischaemia- or anoxia-induced impairment of myocytic structure and cardiac function in the isolated, isovolumicly-contracting, perfused rat heart. 651 60

Myocardial substrate metabolism and enzyme release following hypothermic potassium cardioplegia with and without the addition of mannitol in the cardioplegic solution were studied in two series of patients undergoing isolated aortic valve replacement. Measurements were made of PO2. O2-saturation and content, PCO2, pH, glucose, lactate, pyruvate, potassium, myoglobin, creatine kinase (CK), its isoenzyme MB and aspartate aminotransferase (ASAT) simultaneously in arterial and coronary sinus blood before cardioplegia and during the first 60 min after the release of aortic cross-clamping. In addition, myoglobin and enzymes were followed in peripheral venous blood for 72 hours after cardioplegia. Analysis of the results revealed no striking difference between the groups. Nevertheless, with the addition of mannitol, there was a slightly lower release of lactate and myoglobin probably indicating a more rapid metabolic recovery of the myocardium.
Scand J Thorac Cardiovasc Surg 1981
PMID:Myocardial protection during aortic valve replacement. effects of mannitol in the cardioplegic solution on cardiac metabolism and enzyme release. 680 61

It is demonstrated that plasma elimination constants for rapidly eliminated circulating tissue enzymes can be obtained from plasma time-activity curves if a slowly eliminated reference enzyme is simultaneously sampled. Enzyme and reference enzyme must be released together into the plasma. From the elimination constants thus obtained enzyme release into the plasma can be calculated as a function of time. The method can be applied during continuous release of enzyme into the plasma. The validity of the method is tested in the dog by intravascular infusion of a preparation of cytoplasmic enzymes, obtained by incubating dog liver under anoxic conditions. Alanine aminotransferase (ALT) was used as reference enzyme. Infused quantities of aspartate aminotransferase (AST), glucosephosphate isomerase (GPI) and ALT can be estimated with coefficients of variation (CV) of respectively 10, 19 and 7.6%. Application of the method to plasma time-activity curves of enzymes in patients after acute myocardial infarction (AMI), with alpha-hydroxybutyrate dehydrogenase (HBD) as reference enzyme, results in the following values for the fractional catabolic rate constants (FCR) of AST, GPI, creatine kinase (CK) and its isoenzyme CK(MB): FCRAST = 0.093 +/- 0.006 h-1; FCRGPI = 0.27 +/ 0.03 h-1 (mean +/- SE, n = 14); FCRCK = 0.20 +/) 0.02 h-1 (n = 30); FCRCK(MB) = 0.34 +/- 0.08 h-1 (n = 16). These values are considerably higher than mentioned by most authors, and this indicates that enzyme release after AMI has been underestimated. After AMI, enzymes are released in quantities proportional to the enzyme content of human heart tissue. Average release of CK conforms to this rule but large variations for individual patients are observed. Accurate estimates of the quantities of enzymes released into the plasma can be made for slowly eliminated enzymes by the use of fixed mean values for elimination constants. The results presented to this study indicate that tissue enzymes released from infarcted myocardium in patients after AMI are recovered quantitatively in the plasma. Local inactivation of enzymes or inactivation during the transport from heart to plasma is not significant in such patients.
Cardiovasc Res 1982 Mar
PMID:Quantitative analysis of plasma enzyme levels based upon simultaneous determination of different enzymes. 708 66

Myocardial substrate metabolism and enzyme release following hypothermic potassium cardioplegia were studied in two series of patients undergoing isolated aortic valve replacement. In 15 patients blood was used as cardioplegia vehicle (blood cardioplegia group) and a plain electrolyte solution was used in a control group of 17 patients. Simultaneous blood samples were drawn from arterial and coronary sinus blood before and during the first 60 min after release of aortic cross-clamping. Blood samples were analyzed for PO2. O2-saturation and content, PCO2, pH, lactate, pyruvate, glucose, potassium, myoglobin, creatine kinase (CK), its isoenzyme MB and aspartate aminotransferase (ASAT). In addition, myoglobin and enzymes were followed in peripheral venous blood for 48 hours. The pattern of metabolic changes after cardioplegia was similar in both groups, but some differences were encountered in the degree of the changes in potassium, myoglobin and CK-MB between the groups. The differences were nevertheless small and cell damage was probably of reversible nature in all patients, but the myocardial protection afforded by single dose blood cardioplegia was not unquestionably better than that of the control group.
Scand J Thorac Cardiovasc Surg 1981
PMID:Myocardial protection during aortic valve replacement. Comparison between sanguineous and Asanguineous Cardioplegic Solutions. 733 84


<< Previous 1 2 3 4 5 6 Next >>