Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

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.
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PMID:Distribution of cytosolic and mitochondrial aspartate aminotransferase in normal, ischemic, and necrotic myocardium. An immunohistochemical study. 638 75

Immature, postpubertal, young adult, and middle-aged rats were lightly restrained for 4 h. Relative to untreated controls, restraint uniformly reduced body weight and plasma luteinizing hormone concentration and elevated plasma corticosterone concentration in all age groups. However, restraint increased activities of plasma alanine and aspartate aminotransferase, creatine phosphokinase, and fructose-diphosphate aldolase in only immature and middle-aged animals. This age-related release of tissue enzymes is hypothesized to reflect enhanced responsiveness to catecholamines in immature rats, and possible ischemia related to diminished vasodilatory activity in middle-aged rats. On the basis of these changes, tolerance to restraint in postpubertal and young adults appears to be slightly greater than that of immature and middle-aged rats.
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PMID:Age-related responses to mild restraint in the rat. 664 80

This study was aimed to evaluate the effect of catecholamine on the myocardium reperfused after hypothermic global ischemia, by changes of hemodynamics, biochemistry and ultrastructure. Under cardiopulmonary bypass (CPB) at flow rate 80 ml/kg/min., the aorta was clamped for 60 min. at 28 degrees C of myocardial temperature and reperfused for 60 min. in 26 mongrel dogs. They were divided into 4 groups by infusion of physical saline solution (control), epinephrine 1 microgram/kg/min. (group 1), epinephrine 0.1 microgram/kg/min. (group 2) and dobutamine 5 micrograms/kg/min. (group 3) during reperfusion. The hemodynamic parameters and myocardial isoenzyme (m-AST, MB-CPK) of coronary sinus venous blood were measured before CPB, 30 and 60 min. after declamp. The myocardial adenosine triphosphate (ATP), creatine phosphate (CP), water content, tissue Ca content and fine structure with score of mitochondrial membrane and cristae were examined in epicardium and endocardium at the end of experiment. Hemodynamic parameters after declamp were higher in group 1, 2 and 3 than control (p less than 0.05). The water content and tissue Ca content in group 1 were higher than control. The ATP of endocardium was lowest but CP was no significant difference among four groups. The mitochondrial score in group 1 was lower than control. These data suggest that epinephrine and dobutamine increase hemodynamics and tissue Ca content on the reperfused myocardium following 60 min. of hypothermic global ischemia, but they do not improve depletion of ATP and disruption of myocardial ultrastructure. High dose of epinephrine accentuates ischemic damage of reperfused myocardium after hypothermic global ischemia.
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PMID:[Effect of catecholamine on reperfused myocardium following hypothermic global ischemia]. 674 11

The possible myotoxic effect of bupivacaine in combination with tourniquet ischemia was evaluated in 11 patients who underwent surgery of an arm under intravenous regional anesthesia. Eleven patients with the same kind of surgery and tourniquet who had general anesthesia served as controls. Venous blood bupivacaine concentrations in the anesthetized arm were high at the end of tourniquet time (27.2-202 micrograms/m1) and varied from 2.3 to 12.3 micrograms/ml 10 min after tourniquet release. Changes in blood-gas tensions and plasma potassium and lactate concentrations before and just after tourniquet release correlated with the ischemia time. Changes in creatine phosphokinase, lactate dehydrogenase and aspartate aminotransferase activities, possible indices of loss of integrity of muscle cell membranes, varied considerably and did not correlate with the ischemia time. There were no significant differences between the two groups in any of the parameters. Electron microscopy revealed no evidence of muscle degeneration 24 hr after the use of tourniquet with either bupivacaine intravenous regional (n = 4) or general anesthesia (n = 3).
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PMID:Evaluation of the myotoxicity of bupivacaine in bier blocks--a biochemical and electron microscopic study. 688 67

Observations on early pathophysiology of burning suggests that the release of prostaglandins and thromboxanes plays a role in dermal ischemia. Because of the similarities of the early-phase frostbite wound, blister fluids were aspirated from 10 patients with frostbite, and routine biochemical analysis, immunoelectrophoresis, immunodiffusion, and evaluation of prostaglandins E2, F2 alpha, and thromboxane B2 were performed. Potassium, serum glutamic-oxaloacetic transaminase (SGOT), creatine phosphokinase (CPK), and lactic dehydrogenase (LDH) levels exceeded normal serum values. All blisters were found to have IgM, IgG, IgA, C3a, and opsonin. PgE2 was present in levels less than normal, but PgF2 alpha and TxB2 were markedly elevated. Since the vasoconstricting metabolites of arachidonic acid, PgF2 alpha and TxB2, are known to mediate dermal ischemia in burns and pedicle flaps, it is suggested they may play a role in the pathogenesis of frostbite.
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PMID:Evaluation of hand frostbite blister fluid as a clue to pathogenesis. 720 18

We examined the polyamine metabolism in liver transplanted after cold ischemia and effects of putrescine administration on liver injury, liver regeneration, and survival rate after orthotopic liver transplantation in the rat. Male Wistar rats were used as donors and recipients. Grafts were stored in Euro-Collins solution for 6 h at 4 degrees C. Orthotopic liver transplantation was performed by the three cuff technique. The activities of aspartate aminotransferase, alanine aminotransferase and lactate dehydrogenase elevated and peaked 4 h after liver transplantation. Hepatic ornithine decarboxylase and spermidine/spermine N1-acetyltransferase activities were also elevated and peaked 8 h after the operation. In agreement with the increases in ornithine decarboxylase and spermidine/spermine N1-acetyltransferase activities, the putrescine content increased and spermidine content decreased in the transplanted liver. Putrescine administrated intraperitoneally improved the survival rate, decreased serum transaminase level and increased the [3H]thymidine incorporation into the liver DNA. These findings suggest that both biosynthetic and biodegradative pathways are stimulated in liver transplantation, resulting in the increase in the formation of putrescine from ornithine and from spermidine, and that putrescine administration improve the survival rate by protecting the damaged graft after cold ischemia and reperfusion and by stimulating liver regeneration.
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PMID:Polyamine metabolism in the rat liver after orthotopic liver transplantation. 749 79

The mechanism by which FK506 (FK) prevents hepatic injury induced by ischemia/reperfusion was studied. Adult Sprague-Dawley rats were subjected to 60-min normothermic liver ischemia. Animals were divided into two groups: group I, controls, saline vehicle treatment; group II, FK treatment. FK (1 mg/kg/day, p.o.) was given for 4 consecutive days prior to inducing ischemia. In addition to a survival study, plasma levels of endotoxin and serum activities of tumor necrosis factor-alpha (TNF) and aspartate aminotransferase (AST) were assessed in the blood collected from suprahepatic vena cava. Results showed: (1) FK therapy significantly improved 7-day survival (80.0%) compared with nontreated animals (50.0%, p < 0.05); (2) both TNF and endotoxin were elevated following reperfusion, reaching maximum values at 3 h after reperfusion (217.0 +/- 40.6 and 280.5 +/- 31.4 pg/ml, respectively, in the control; mean +/- SEM), and (3) serum activities of TNF and AST following reperfusion were substantially suppressed with FK treatment, whereas FK did not reduce the rise in endotoxin. These findings suggest that suppression of TNF production in response to endotoxemia might account at least in part for the protective effect of FK against ischemia-induced hepatic injury.
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PMID:Evidence that FK506 alleviates ischemia/reperfusion injury to the rat liver: in vivo demonstration for suppression of TNF-a production in response to endotoxemia. 751 91

In order to study further whether a relationship exists between the extent of ischemia-preservation-reperfusion injury (IPRI) and acute rejection (AR) events in liver allografts, we retrospectively reviewed 213 consecutive cyclosporine-treated patients who received their first liver allograft between 1/1/93 and 12/31/93. Of these, 178 fulfilled the study inclusion criteria. The extent of IPRI was assessed by the peak value of aspartate aminotransferase (ASTmax) observed within the first 72 hr posttransplant. For the purpose of univariate analysis, categorical classification of recipients was done based upon ASTmax as follows: group 1, ASTmax < 600 IU/L (n = 43); group 2, ASTmax 600-2000 IU/L (n = 86); and group 3, ASTmax > 2000 IU/L (n = 49). For multivariate analysis, stepwise Cox regression was performed with age, ASTmax, and UNOS status as covariates. At a median follow-up of 271 days there were no statistically significant differences between groups with respect to the incidence of a first episode of AR (47%, 55%, 51%, respectively, P = NS), the timing of AR (respective medians, 9, 10, and 10 days, P = NS), or the proportion of patients treated with OKT3 (9%, 20%, 12%, respectively, P = NS) or converted to FK506 (16%, 12%, 10%, P = NS). Cox regression confirmed the lack of an independent association between the extent of IPRI and any of these outcomes. We conclude that in UW-preserved, cyclosporine-treated primary liver allografts, no correlation exists between the extent of IPRI and the incidence, timing, severity, or refractoriness of clinically defined AR events.
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PMID:Lack of correlation between the magnitude of preservation injury and the incidence of acute rejection, need for OKT3, and conversion to FK506 in cyclosporine-treated primary liver allograft recipients. 757 Sep 50

The degree of residual liver injury in normal and cirrhotic rats undergoing 70% hepatectomy with hepatic inflow occlusion was examined. The total duration of clamping was 60 min and animals were divided into 3 groups according to the ischemic modality: a 15-min intermittent clamping group (group I); a 30-min intermittent clamping group (group II), and a 60-min continuous clamping group (group III). In normal liver rats, the survival rates after operation in groups I, II and III were 90, 90 and 30%, respectively, compared to 70, 50 and 38%, respectively, in cirrhotic rats. The serum aspartate aminotransferase (AST) level increased markedly with prolongation of each period of clamping in rats with normal liver, showing higher AST levels than those with cirrhotic liver. The liver tissue adenosine-5'-triphosphate (ATP) levels and energy charge (EC) values decreased with prolongation of each period of clamping. Cirrhotic livers showed lower ATP levels and EC values than normal livers. Although there was no significant difference in the mitochondrial function between normal and cirrhotic livers in the group of the same form of ischemia, phosphorylative efficiency of mitochondria was maintained satisfactorily in normal groups I and II and in the cirrhotic group I. Even though cirrhotic livers showed a smaller necrotic response to ischemia than normal livers, they were more vulnerable to ischemia because of an inability to maintain energy metabolism. Therefore, when performing resection of a cirrhotic liver, a 15-min intermittent clamping method should be adopted.
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PMID:Experimental study of liver injury after partial hepatectomy with intermittent or continuous hepatic vascular occlusion. Differences in tolerance to ischemia between normal and cirrhotic livers. 758 3

The liver has been judged relatively resistant to ischemia, but prolonged inflow occlusion at normothermic conditions can produce evidence of reversible or irreversible hepatocellular damage. Cytoprotective agents have been used both experimentally and clinically to afford extended viability of hepatocytes under reduced perfusion. One agent, prostaglandin E1, has been described clinically as effective in sustaining liver function under ischemic conditions. We have sought to verify this observation in an experimental model using prolonged normothermic inflow occlusion. Twenty miniature pigs were anesthetized and subjected to subtotal normothermic hepatic inflow occlusion (portal vein, hepatic artery, choledochal vessels) to allow for sufficient splanchnic decompression. Half of the animals received pretreatment with prostaglandin E1 (alprostadil) 500 micrograms intravenously. Inflow occlusion was maintained for 2 hours followed by reperfusion and killing 24 hours later. As a measure of functional preservation, the tissue adenine nucleotides adenosine monophosphate, diphosphate, and triphosphate (AMP, ADP, ATP) were measured in ischemic liver by freeze-clamping and high-performance liquid chromatography during occlusion and after reperfusion. Cytosolic enzyme determinations (aspartate transaminase, alanine transaminase, lactate dehydrogenase) were also made before occlusion and after reperfusion. As a possible indicator of cellular injury, blood ionized Ca++ was measured before inflow occlusion and after reperfusion. Although no difference was found in levels of AMP and ADP between prostaglandin E1 and control animals, ATP levels rose significantly higher during recovery in prostaglandin E1 animals at 60 minutes and 24 hours after reperfusion (13.97 +/- 1.29 and 13.60 +/- 0.91 mumoles/gm dry weight prostaglandin E1 vs. 9.25 +/- 0.97 and 9.80 +/- 0.85 mumoles/gm dry weight co control, P < .01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of prostaglandin E1 on liver adenine nucleotides and cytoplasmic enzymes in a porcine model of normothermic hepatic ischemia. 759 Jun 75


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