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)

The effects of myocardial reperfusion have been examined following a 1 h coronary occlusion and compared to a permanent coronary ligation in pigs. Haemodynamic investigations were carried out throughout the surgical intervention and repeated after 7 days. Cellular injury was estimated by serial serum enzyme determinations (creatin phosphokinase, alpha-hydroxybutyric dehydrogenase, aspartate aminotransferase, lactic dehydrogenase) during the first 5 postoperative days; infarct size was assessed morphometrically by a histochemical staining procedure 1 week after the temporary or permanent coronary occlusion. A linear correlation was found between the logarithmically plotted peak serum activity of AST, HBDH, CPK and the morphometrically determined infarct size. Based upon enzyme and morphometrical studies no significant difference could be detected between the two experimental groups. In the animals subjected to transient coronary occlusion, however, the development of a ventricular aneurysm had been prevented to early and sustained reperfusion. Early re-establishment of coronary circulation appears to accelerate the proliferation of a more resistant granulation tissue into the infarcted area. Cardiac performance was not improved by myocardial reperfusion.
 ...
PMID:Consequences of myocardial reperfusion following temporary coronary occlusion in pigs; effects on morphologic, biochemical and haemodynamic findings. 41 74

The activity of alpha-hydroxybutyrate dehydrogenase, creatine kinase, creatine kinase MB and aspartate aminotransferase was measured on serial plasma samples from patients with acute myocardial infarction. The study was part of a multicentre randomised trial of the effect of thrombolytic treatment in the acute phase of acute myocardial infarction. The applicability and comparability of enzyme tests for the estimation of myocardial injury were studied in 76 control patients and 74 patients treated with streptokinase. Treatment with streptokinase caused a considerable acceleration of enzyme release after acute myocardial infarction, both in patients with persistent coronary occlusion and in those with successful reperfusion. But this changed pattern of enzyme release did not affect the rate of enzyme elimination from plasma or the released proportions of different enzymes. Thus the assessment of infarct size by measurement of these enzyme activities can also be applied to patients treated with streptokinase. Moreover, the enzymes measured in the present study are all equally valid markers of myocardial injury.
 ...
PMID:Enzyme tests in the evaluation of thrombolysis in acute myocardial infarction. 334 58

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

The present study was performed to evaluate the cardioprotective effects of [5-(2-methoxy-5-chloro-5-phenyl)furan-2-ylcarbonyl]guanidine (KR-32570) in rat and dog models of coronary artery occlusion and reperfusion. In addition, we sought to clarify the efficacy of KR-32570 on reperfusion-induced fatal ventricular arrhythmia. In anesthetized rats subjected to 45-min coronary occlusion and 90-min reperfusion, KR-32570 (i.v. bolus) dose-dependently reduced myocardial infarct size from 58.0% to 50.7%, 35.3%, 33.5% and 27.0% for 0.03, 0.1, 0.3 and 1.0 mg/kg, respectively (P<0.05). In anesthetized beagle dogs that underwent 1.2-h occlusion followed by 3.0-h reperfusion, KR-32570 (3 mg/kg, i.v. bolus) markedly decreased infarct size from 28.9% in vehicle-treated group to 8.0% (P<0.05), and reduced the reperfusion-induced release in creatine kinase isoenzyme MB, lactate dehydrogenase, Troponin-I and glutamic-oxaloacetic transaminase. KR-32570 dose-dependently decreased the incidence of premature ventricular contraction, ventricular tachycardia or ventricular fibrillation induced by ischemia and reperfusion in rats. Similar results were obtained in dogs with reperfusion-induced arrhythmia. In separate experiments to assess the effects of timing of treatment, KR-32570 given 10 min before or at reperfusion in rat models also significantly reduced the myocardial infarct size (40.9% and 46.1%, respectively) compared with vehicle-treated group. In all studies, KR-32570 caused no significant changes in any hemodynamic profiles. Taken together, these results indicate that KR-32570 significantly reduced the myocardial infarction and incidence of arrhythmias induced by ischemia and reperfusion in rats and dogs, without affecting hemodynamic profiles. Thus, it could be potentially useful in the prevention and treatment of myocardial injuries and lethal ventricular arrhythmias.
 ...
PMID:Effects of KR-32570, a new sodium hydrogen exchanger inhibitor, on myocardial infarction and arrhythmias induced by ischemia and reperfusion. 1622 44