Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.6.1.2 (alanine aminotransferase)
 26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adult male and female Sprague-Dawley rats were subjected to an isoproterenol-induced myocardial infarction. Six weeks before the induction of myocardial infarction, some of the animals had been orchiectomized or ovariectomized. The animals were autopsied at regularly timed intervals on days 1, 2, 3, 8, and 15 after myocardial infarction. The gonadectomized animals manifested less severe untoward changes, survived in greater numbers, and experienced superior repair of their damaged hearts. Circulating levels of enzymes (e.g., CPK, GOT, GPT, and LDH), lipids, glucose, and BUN rose and fell during the acute necrosis and repair phases with distinct differences between the intact and castrated animals. Reciprocal changes in the weight of the adrenal and thymus glands, coupled with dynamic changes in circulating corticosterone levels, reflected marked temporal changes in the spectrum of adrenal steroids being secreted, as well as gonadal hormone mediated changes affecting adrenocortical function. The implications of these findings are that adrenocortical, androgenic, and estrogenic hormones condition the nature of the pathophysiologic response to acute myocardial infarction in rats.
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PMID:Effect of gonadectomy on isoproterenol-induced myocardial infarction. 45 39

Myoglobin and the enzymatic activity of creatine phosphokinase CK), MB-isoenzyme of CK (CK-MB), aspartate aminotransferase (GOT), alanine aminotransferase (GPT) and lactic acid dehydrogenase (LDH) were serially determined in 10 patients with acute myocardial infarction. Additionally the same parameters were assessed in 5 patients with angina pectoris for 24 hours after bicycle ergometry. 10 in-patients served as controls. Myoglobin was determined by radioimmunoassay and the other enzyme activities according to the current kinetic methods. Comparison of myoglobin with the enzymatic parameters showed that the myoglobin peak occurs 5.6 hours after the beginning of the sampling period, i.e. 7.3 hours earlier than CK and CK-MB and 11.6 hours earlier than GOT. In analogy to this finding the descending limb of the myoglobin curve was significantly earlier at a level of one third of the peak value, i.e. 8.2 hours earlier than CK-MB, 18.8 hours earlier than CK and 27.3 hours earlier than GOT. No signs of myocardial necrosis in terms of myoglobin or enzymatic activity could be detected after bicycle ergometry. It is concluded that myoglobin is a more sensitive parameter for assessment of the acute phase in patients with myocardial infarction than the usualy enzymatic parameters.
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PMID:[Plasma myoglobin level as a course criterium in patients with acute myocardial infarct]. 53 58

Two groups of 23 patients, each with acute myocardial infarction, were treated. The first group (control) received glucose-insuline-K+ (GIK) over a 3-day period, and the second GIK and N-methyl-N-(beta-hydroxyethyl) guanidine O-phosphate (creatinol O-phosphate, COP) (3.06 g i.v./24 h), again for a 3-day period. The six enzymes investigated, i. e. GOT, GPT, LDH, HBDH, CK and MBCK, all decreased between 33 and 49% in the COP group as compared with the control group, reaching a degree of statistical significance of less than 0.01. The decrease in these enzymes was attributed to the protective action of COP on the cell membrane permeability, in agreement with a series of previous papers.
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PMID:Effects of creatinol O-phosphate on serum enzymes in acute myocardial infarction. 57 98

In a group of 113 consecutive patients taken into a coronary care unit on suspicion of acute myocardial infarction, blood samples were taken every 6 h and the following enzyme activities were measured: creatine kinase (S-CK), aspartate aminotransferase (S-ASAT), alanine aminotransferase (S-ALAT) and lactate dehydrogenase (S-LD). All measurements were made according to the Recommendations of the Scandinavian Committee on Enzymes. On all patients S-CK B subunit activity was determined by immunoinhibition with a specific anti CK M-subunit inhibitory antibody. At peak values of the respective total enzyme activities CK and LD isoenzymes were further qualitatively estimated by electrophoresis. The data indicate that even serial determinations of total CK, ASAT, ALAT and LD activities in serum do not provide the information required for a conclusive diagnosis of myocardial infarction in the individual case. In contrast, the positive predictive value (PV) of S-CK B was found to be 1.0 and the negative predictive value was 0.98. S-CK MB showed a PV pos. of 1.0 and also a PV neg. of 1.0. Electrophoretic determination of S-LD isoenzymes was slightly poorer with a PV pos. of 0.96 and PV neg. of 0.98. S-CK, total activity with nearly 9 per cent false positives had a positive predictive value of only 0.91, but a negative one of 1.0.
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PMID:Creatine kinase B-subunit activity in human serum. II. Evaluation of s-ck b-subunit activity in the diagnosis of acute myocardial infarction. 88 49

With the purpose of determining the long and short term changes in serum enzyme activities after a marathon race, a survey involving nine healthy male runners was carried out. A basal blood sample was extracted from each 24 hours prior to the race and three further extractions were made immediately after the race, as well as at 1 and a final 24 h after the end of the race. In the enzymes of preferably hepatic origin--alkaline phosphatase (AP), ganna-glutamyltransferase (GGT) and alanine aminotransferase (ALT)--scanty modifications were found and these could be related to the changes observed in the plasma volume. Enzymes such as aspartate aminotransferase (AST) and lactate dehydrogenase (LDH), which are widely distributed in the tissues, were found to have undergone more marked variations and these could not be related to the changes in the volume of the plasma, while in enzymes of muscular origin such as aldolase (ALD), creatine kinase (CK) and its cardiac isoenzyme (CK-MB), notable increases were observed due to the muscular injury suffered. The greatest example of this was the increase found in total CK 24 h after the end of the marathon (414.6%). The high serum percentages found in CK-MB in these endurance-trained runners in relation to total CK activity should be carefully assessed in order to avoid false diagnosis of acute myocardial infarction.
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PMID:Serum enzymes activities at rest and after a marathon race. 143 88

Current therapy of myocardial infarction may include early reperfusion. We simulated myocardial perfusion conditions during evolving myocardial infarction in isolated, normothermic, isovolumic rabbit hearts perfused with buffer containing bovine red blood cells (hematocrit of 40%), and we assessed the effects of high levels of glucose and insulin as "therapy" during prolonged (150-minute) severe underperfusion and reperfusion. Protocol 1 consisted of underperfusion at a constant coronary perfusion pressure of 8 mm Hg. The control group (n = 8) received 5.5 mmol/l glucose and 15 microunits/ml insulin; the group treated with high levels of glucose and insulin (G + I) (n = 8) received 19.5 mmol/l glucose and 250 microunits/ml insulin during both underperfusion and reperfusion. Relative to the control group, the G + I group experienced 1) greater developed pressure during underperfusion and increased recovery during reperfusion, 2) preserved diastolic function during underperfusion and reperfusion, 3) lower coronary resistance and greater coronary flow during the underperfusion period, 4) increased glycolytic flux and preserved glycogen stores and high energy phosphate levels, and 5) less loss of myocyte enzymes (creatine kinase and alanine aminotransferase). In protocol 2, coronary flow was kept identical in control (n = 8) and G + I hearts (n = 8) during the underperfusion period, and left ventricular end-diastolic pressure was kept below 10 mm Hg in both groups to minimize subendocardial damage and vascular compression. In this protocol, the effect of the G + I intervention in the prevention of an increase in coronary resistance during the underperfusion period was distinguished from its myocellular metabolic effects; the high G + I substrate had protective effects on mechanical and metabolic function that were less marked than, but similar to, those in protocol 1, indicating that its mechanisms of protection during underperfusion affected both cardiac function and coronary resistance. We conclude that the G + I intervention, in clinically relevant concentrations, markedly protected severely underperfused myocardium for 150 minutes and may be a beneficial intervention in combination with reperfusion therapy in acute myocardial infarction.
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PMID:Protective effect of increased glycolytic substrate against systolic and diastolic dysfunction and increased coronary resistance from prolonged global underperfusion and reperfusion in isolated rabbit hearts perfused with erythrocyte suspensions. 199 51

Early increases in the activity of alanine aminotransferase (ALT, EC 2.6.1.2) in plasma are observed in about 7% of patients with acute myocardial infarction (AMI), of whom about half die. Some type of liver injury, secondary to AMI, could be responsible for this phenomenon. However, quantitative analysis shows that the release of ALT in most of these patients conforms to the myocardial release pattern. Moreover, extra release of hepatic aspartate aminotransferase (EC 2.6.1.1) is not observed. These findings suggest that the heart may occasionally contain a high ALT activity. This hypothesis was verified by determination of enzyme activities in 10 hearts obtained from patients who died after AMI. The mean ALT activity in these hearts, 21 (SD 12) U per gram wet weight, significantly (P less than 0.01) exceeds the value of 7.7 (SD 4.9) U/g found for seven control hearts and may reflect increased amino acid metabolism in the energy-depleted heart muscle, as described earlier for skeletal muscle.
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PMID:Greater than expected alanine aminotransferase activities in plasma and in hearts of patients with acute myocardial infarction. 291 73

Fifty-four patients with acute myocardial infarction were evaluated repeatedly, with 28 of those treated with piracetam, and 26 used as controls. Piracetam produced a considerable favorable effect on the clinical course of myocardial infarction, as reflected in a more rapid clinical improvement of acute circulatory insufficiency and an analgetic effect. The drug reduced heart rate and moderately elevated systolic arterial blood pressure. Positive changes in total CPK, LDH, AST and ALT activities, and in ECG from 12 and 35 leads were quicker to come.
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PMID:[Therapeutic use of piracetam in myocardial infarct patients]. 357 22

A rapid selective method for measuring the activity of lactate dehydrogenase isoenzyme LD-1 in serum by using 1,6-hexanediol as an inhibitor of the M-subunit was developed. Hexanediol was added to serum at a final concentration of 0.7 mol/l. After incubation at 30 degrees C for 15 min, the activity was measured with an automatic analyser. The inter-assay coefficient of variation was 6.9% for the lactate dehydrogenase isoenzyme LD-1 measurement. The results obtained from the sera of 100 patients analysed by the proposed selective method and by the conventional electrophoretic method, respectively, showed an excellent correlation. This selective method was used to determine the lactate dehydrogenase isoenzyme LD-1 activity of sera from patients with acute myocardial infarction, and the results were correlated well with those obtained by the immunological, Roch Isomune method. Addition of 1,6-hexanediol did not affect the measurement of activities of other enzymes such as alkaline phosphatase, gamma-glutamyltransferase, aspartate aminotransferase and alanine aminotransferase.
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PMID:Selective determination of lactate dehydrogenase isoenzyme 1 in serum after inhibition by 1,6-hexanediol. 369 31

The occurrence of liver damage was investigated in patients with uncomplicated acute myocardial infarction (AMI). Cumulative plasma release of creatine kinase (CK) and alpha-hydroxybutyrate dehydrogenase (HBD) was compared with release of alanine aminotransferase (ALT). Up to 48 h after AMI, the appearance of ALT could be fully explained by myocardial ALT release. Thereafter additional release of ALT occurred, indicating liver damage. A possible effect of liver function on the rate of elimination of CK from plasma was studied in the dog. Complete temporary arrest of hepatic blood supply was obtained after previous implantation of a portacaval shunt, ligation of secondary inflows and blockade of retrograde perfusion. Neither these preliminary haemodynamic interventions nor the acute arrest of hepatic blood flow had any effect on the disappearance rate of CK from plasma. It is concluded that some liver damage commonly occurs in patients after AMI. However, this phenomenon does not interfere with the estimation of infarct size because the elimination of CK from plasma is unaltered during total hepatic ischaemia.
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PMID:Liver damage as a potential source of error in the estimation of myocardial infarct size from plasma creatine kinase activity. 397 66


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