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

In a consecutive series of 25 coronary bypass operations, the postoperative serum activity levels of total creatine kinase (CK) and its more heart-specific isoenzyme CK-MB were examined and related to the levels of aspartate aminotransferase (ASAT), alanine aminotransferase (ALAT) and thermostable lactate dehydrogenase (LD-T), to electrocardiographic (ECG) findings and to surgical characteristics. Detectable CK-MB activity was found in all patients, usually appearing while the operation was still in progress. Peak CK-MB occurred earlier than peak total CK. There was no ECG evidence of myocardial infarction in any patient. The degree of postoperative CK-MB elevation, however, correlated to the duration of extracorporeal circulation (ECC) and aortic cross-clamping (AC). After 120 min of ECC and 70 min of AC, release of CK-MB, as well as of the other enzymes studied, increased considerably. There was a significant correlation between high CK-MB activity and high early postoperative activities of total CK, ASAT and LD-T. When CK-MB determinations are not available, ASAT is preferable to total CK or LD-T in the early evaluation of operative myocardial injury. From the fourth postoperative day, only LD-T is informative in this respect; a second rise of ASAT and ALAT is probably of hepatic origin.
Scand J Thorac Cardiovasc Surg 1979
PMID:Serum enzymes with special reference to CK-MB following coronary bypass surgery. 31 43

This retrospective analysis tests the hypothesis that topical cardiac hypothermia is an unnecessary adjunct to intraoperative myocardial protection and an avoidable cause of pulmonary morbidity in patients with coronary disease receiving blood cardioplegia. The hospital records of 150 nonrandomized consecutive patients undergoing elective and emergency isolated coronary revascularization were reviewed. All patients received multidose cold blood cardioplegia followed by warm blood cardioplegic reperfusion distributed through grafts. Fifty patients received iced slush, 50 received topical 4 degrees C saline, and no topical cooling was used in 50 others. Patients groups were comparable in number of grafts (3.7 versus 3.5 versus 3.5) and crossclamp time (61 versus 62 versus 61 minutes). More emergency operations were performed in the patients receiving no topical hypothermia (12/50 versus 8/50 versus 7/50). Postoperative x-ray films were reviewed by a radiologist who did not know of patient grouping. Postoperative results were comparable in hemodynamics, inotropic requirements (10/50 ice versus 8/50 saline versus 5/50 no cooling), myocardial infarction (1/50 versus 2/50 versus 2/50), and enzymes (aspartate aminotransferase myocardial band creatine kinase). No patient died. Ice topical hypothermia (versus no topical cooling) was associated with more left pleural effusions (25/50 versus 9/50; p less than 0.05), atelectasis (33/50 versus 18/50; p less than 0.05), elevated left hemidiaphragms (13/50 versus 0/50; p less than 0.05), and longer postoperative hospitalization (11.2 versus 8.5 days; p less than 0.05). Topical 4 degrees C saline reduced diaphragmatic elevation and pleural effusion (versus topical ice) but was associated with more atelectasis (34/50 versus 18/50; p less than 0.05) than no topical cooling. These data suggest that routine topical hypothermia is an unnecessary adjunct to blood cardioplegic protection in patients with coronary disease, since supplemental topical cooling does not improve postoperative hemodynamics or reduce inotropic requirements, enzyme release, or prevalence of postoperative myocardial infarction, and it increases pulmonary morbidity, which can be reduced by its avoidance.
J Thorac Cardiovasc Surg 1992 Sep
PMID:Topical cardiac hypothermia in patients with coronary disease. An unnecessary adjunct to cardioplegic protection and cause of pulmonary morbidity. 151 52

We have previously shown the safety and efficacy of University of Wisconsin solution for hypothermic preservation of the human donor heart in a pilot group of 16 transplant recipients. The present study is a randomized clinical trial comparing University of Wisconsin solution to conventional preservation using crystalloid cardioplegia and saline storage within a 4-hour limit of ischemia. Heart transplant recipients (n = 42) were randomized into two groups: those receiving hearts preserved by University of Wisconsin solution, the UWS group (n = 22), and those receiving hearts preserved in the conventional manner, the CCS group (n = 20). Recipient age, gender, heart disease, and preoperative inotropic support and donor age, gender, and mean ischemic time in hours (UWS 2 hours 36 minutes, range 1 hour 36 minutes to 2 hours 53 minutes; CCS 2 hours 20 minutes, range 1 hour 20 minutes to 2 hours 44 minutes; p = not significant) were similar. Significant differences observed between the two groups included (1) mean time (minutes) from reperfusion to achieve a stable rhythm, (2) need for intraoperative defibrillations, (3) need for transient cardiac pacing, and (4) integrated postoperative creatinine kinase and aspartate aminotransferase release over 48 hours. There was no difference in postoperative electrocardiogram, endomyocardial biopsy, or hemodynamics. One UWS patient died of sepsis and another of a ruptured cerebral aneurysm. UWS is safe for donor organ arrest and preservation despite high viscosity and potassium concentration. When compared with CCS hearts, hearts preserved in UWS regained electrical activity more rapidly and had better myocardial protection as demonstrated by enzymatic analysis. Further investigation is required to determine the effects of UWS preservation on long-term survival, to determine the prevalence of rejection and graft atherosclerosis, and to test the ability of UWS to extend donor ischemic time in human cardiac transplantation.
J Thorac Cardiovasc Surg 1992 Feb
PMID:University of Wisconsin solution versus crystalloid cardioplegia for human donor heart preservation. A randomized blinded prospective clinical trial. 173 83

This study explored myocardial protective effects of allopurinol at various doses. Ninety patients undergoing coronary artery bypass or repair or replacement of cardiac valves were divided into three groups of 30 patients each in accordance with the amount of allopurinol administered to patients in each group. Patients in group I received no allopurinol, those in group II received low-dose allopurinol (total dose 1200 mg), and those in group III received high-dose allopurinol (total dose 2400 mg). Aspartate aminotransferase, cardiac isoenzyme of creatine kinase, and lactic dehydrogenase levels were measured up to 5 days after operation. Concentrations of allopurinol and oxypurinol were also measured before initiation of cardiopulmonary bypass and at the start and at the end of aortic crossclamping. Postoperative aspartate aminotransferase, creatine kinase, and lactate dehydrogenase 1 plus lactate dehydrogenase 2 levels in group III were significantly lower than those in groups I and II. Aspartate aminotransferase, creatine kinase, and lactate dehydrogenase 1 plus lactate dehydrogenase 2 levels in group II were lower than those in group I, without statistically significant differences. Plasma oxypurinol concentrations were significantly higher in group III than in group II. It was concluded that allopurinol had resultant high myocardial protective effects in dose-related fashion, but its effect might be attributed to oxypurinol levels formed by its degradation.
J Thorac Cardiovasc Surg 1991 Apr
PMID:A clinical trial of allopurinol (Zyloric) for myocardial protection. 200 10

We investigated whether clinical and laboratory variables can predict perfusion status after t-PA administration, by using the data from 138 patients who received t-PA during the Thrombolysis in Myocardial Infarction (TIMI) I study. All clinical and laboratory variables that were collected at baseline or during perfusion for TIMI I were evaluated by the current study. Via stepwise discriminant analysis, 7 variables were closely associated with perfusion status at 90 minutes (listed in the order of their discriminant effect): baseline grade of stenosis in the infarct-related coronary artery, whether nausea was present during the infusion, baseline aspartate aminotransferase (SGOT) concentration, whether arrhythmias were present during the infusion, baseline fibrinogen concentration, baseline partial thromboplastin time, and baseline diastolic blood pressure. Baseline severity of stenosis and the likelihood of there being reperfusion were inversely related. Eighty-four percent of patients with adequate perfusion after 90 minutes of t-PA infusion were classified correctly, but only 50% of those without perfusion at 90 minutes were classified correctly. In addition, since 70% of the TIMI I patients, on average, did achieve perfusion, the use of these 7 variables added little predictive information. Our findings suggest that 1) there is as yet no practical way to predict reperfusion after t-PA therapy and 2) the severity of coronary stenoses, if known ahead of time, should be considered when selecting patients for thrombolytic therapy.
Cathet Cardiovasc Diagn 1990 Jun
PMID:Prediction of coronary artery reperfusion after tissue plasminogen activator infusion. 211 85

This study tests the importance of amino acid transamination in determining the tolerance of immature hearts to ischemic damage. Amino acid transamination was inhibited metabolically by pretreatment with aminooxyacetic acid. The aminooxyacetic acid dose and duration were determined by incubating in vitro tissue homogenate and showing that an 8 mmol/L AOA dose for 5 minutes blocked 90% of alanine aminotransferase and aspartate aminotransferase activity. Control studies in nonischemic hearts showed that coronary perfusion with aminooxyacetic acid for 5 minutes did not impair myocardial performance. In contrast, pretreatment of immature puppies with aminooxyacetic acid severely impaired recovery after 45 minutes of normothermic global ischemia (30% versus 85% recovery in untreated hearts, p less than 0.05). Biochemical analyses of hearts undergoing ischemia showed aminooxyacetic acid to limit lactate production, impair glutamate utilization, prevent alanine production, and limit succinate accumulation (p less than 0.05). These data suggest that amino acid transamination is an important adaptive process in the immature heart that improves its resistance to ischemic damage.
J Thorac Cardiovasc Surg 1990 Dec
PMID:Studies of myocardial protection in the immature heart. II. Evidence for importance of amino acid metabolism in tolerance to ischemia. 224 11

Prevention of myocardial cell death is an important goal in the treatment of myocardial infarction. The potential benefit of chlorpromazine in myocardial injury was assessed in the isolated rabbit heart under conditions of the calcium paradox. A period of 20 min of calcium-free perfusion followed by reintroduction of calcium was associated with myocardial damage, as indicated by severe impairment in left ventricular contractile function and marked loss of protein and enzymes (aspartate aminotransferase) from the myocardium. Chlorpromazine, 15 or 25 mg/kg, was given intravenously 30 min before excision of the heart. Chlorpromazine was associated with significant (p less than 0.05) improvement in left ventricular function, as indicated by larger developed pressure, greater peak positive and negative dP/dt, and lower left ventricular end-diastolic pressures. Chlorpromazine pretreatment was associated with significant (p less than 0.05) reduction in the amount of enzyme and protein lost from the myocardium. Thus, chlorpromazine can reduce the severity of myocardial cell injury.
J Cardiovasc Pharmacol 1987 Apr
PMID:Effect of chlorpromazine on myocardial damage in the calcium paradox. 243 12

A new method for vital staining of the conduction system during heart operations, the iodine gas method, was used in 12 patients. The right bundle branch stained well in all cases, and could be confirmed by the naked eye. The conduction system was not damaged by the staining procedure. The iodine gas used in this method had no adverse effects on thyroid function (thyroxine, triiodothyronine, thyroxine binding globulin, protein bound iodine) or liver function (serum glutamate oxaloacetate transaminase, serum glutamate pyruvate transaminase, lactic dehydrogenase). This method, therefore, was found to be valuable and without complication for preventing conduction disturbances during cardiac operations.
J Thorac Cardiovasc Surg 1988 Apr
PMID:Clinical application of a new vital staining method for the conduction system during heart operations. 245 Oct 90

The effects of aprotinin on canine myocardium subjected to cardioplegia and global ischemia for 4 hours and then reperfused for 1 hour were investigated. Lysosomal and mitochondrial enzymes and cyclic nucleotides (adenosine cyclic monophosphate and guanosine cyclic monophosphate) were measured in coronary sinus blood. Aprotinin was given intravenously before cardiopulmonary bypass at total doses of 10 X 10(3) kallikrein units per kilogram (group A, six dogs) and 20 X 10(3) KU/kg (group B, six dogs). In group A, three dogs survived but with poor cardiac function; all dogs in group B survived and had better cardiac function. Lysosomal (N-acetyl-beta-D-glucosaminidase) and mitochondrial (aspartate aminotransferase) enzymes in coronary sinus blood at 60 minutes of reperfusion were significantly (p less than 0.05) lower in group B than in group A. In both groups, guanosine cyclic monophosphate was significantly (p less than 0.01) lower during reperfusion than before cardiopulmonary bypass; however, the values were significantly (p less than 0.05) higher in group B than in group A. Serum adenosine cyclic monophosphate was lower during reperfusion than before bypass in both groups, but it recovered during reperfusion in group B. Myocardial adenosine triphosphate was well preserved in both groups but creatine phosphate was decreased (p less than 0.01) in group A. These results suggest that aprotinin at a dose of 20 X 10(3) KU/kg may be effective in preserving myocardial viability and function after prolonged cardioplegia.
J Thorac Cardiovasc Surg 1988 Aug
PMID:Role of protease inhibition in myocardial preservation in prolonged hypothermic cardioplegia followed by reperfusion. Effect of aprotinin in an experimental model. 245 28

Recent investigations have shown that cardiac isoenzymes change with mechanical overload and possibly with myocardial ischaemia. This complicates the interpretation of serum enzyme changes in acute myocardial infarction. We have therefore investigated the rate of release of isoenzymes from necrosing myocardium and the effect of ischaemia per se. Discrete myocardial infarction was produced in 35 male Wistar rats by ligation of left coronary artery. Six (n = 7), 12 (n = 6), 24 (n = 9), 72 (n = 7) h and 3 weeks (n = 6) after surgery, total and isoenzyme activities of creatine kinase (CK), lactate dehydrogenase (LD) and aspartate aminotransferase (AST) were measured in the infarcted myocardium. Untreated rats (n = 12) were used as the control (time 0). Sham operation was performed in 36 rats. During the early period (0 to 12 or 24 h) of infarction, each (iso)enzyme disappeared monoexponentially from the myocardium (mean r = 0.88) with different disappearance rates. Cytosolic isoenzyme fractions decreased more rapidly than mitochondrial fractions. CK MB and the LD-H subunit decreased faster than CK MM and the LD-M subunit. Such differences in the disappearance rate may be related to subcellular localisation of each isoenzyme. In the late period (72 h and 3 weeks), CK BB and the LD-M subunit showed significant reaccumulation in the infarcted myocardium. Although inflammatory cells can be responsible for the reaccumulation of LD-M subunit, the origin of CK BB is unknown.(ABSTRACT TRUNCATED AT 250 WORDS)
Cardiovasc Res 1989 Mar
PMID:Disappearance and appearance of isoenzymes of creatine kinase, lactate dehydrogenase and aspartate aminotransferase in the myocardium undergoing infarction. 259 Sep 8


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