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:2.6.1.2 (alanine aminotransferase)
26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The protective effects of PGE1 on ischemia-related liver damage were evaluated in dogs. Ninety minutes warm hepatic ischemia was induced by the total clamping of hepatic inflow vasculatures with portal bypassing. The survival rate improved up to 62.5% when PGE1 was administered intravenously prior to ischemia, while no dog survived for longer than 1 week in the nontreated group. Hepatic ATP content was restored up to 80% of preischemic level 2 h after reflow in the PGE1 pretreated group, compared to 55% recovery in the nontreated group. Complete normalization of hepatic energy charge and rapid decrease of lactate were also seen in the PGE1 group. The clearance rate of intravascular lipid emulsion remained fairly normal in the PGE1 group, thereby suggesting well-preserved hepatic reticuloendothelial functions. The serum activities of beta-glucuronidase, GOT and GPT were suppressed in the PGE1-pretreated group, thereby implying a well-protected hepatic integrity. The histology revealed well-preserved hepatic architecture. The remarkable cytoprotective effect of PGE1 on hepatic ischemia shown in this study indicates that PGE1 warrants further study for protection of ischemically compromised hepatic allografts.
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PMID:Protective effect of prostaglandin E1 (PGE1) on energy metabolism and reticuloendothelial function in the ischemically damaged canine liver. 292 40

Extensive hepatic necrosis was produced in rabbits 48 hr following infusion of a cardiopathogenic dose of norepinephrine (NE, 2 micrograms/kg/min for 90 min). Livers had necrotic areas of varying sizes and gross appearances. Histologically, the lesions were areas of varying sizes and gross appearances. Histologically, the lesions were areas of lytic-coagulative necrosis with massive mineralization by calcium. In addition, the serum glutamate-pyruvate transaminase (GPT) was significantly elevated (P less than 0.001). Pretreatment with the alpha 1-adrenoceptor blocker prazosin (200 micrograms/kg) 15 min prior to the standard NE infusion prevented both liver necrosis and serum GPT elevation. It is concluded that large doses of NE produce tissue injury in the liver. This may be the result of excessive activation of the alpha 1-adrenoceptor system, which leads to hepatic ischemia and necrosis.
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PMID:Hepatic necrosis induced by norepinephrine in rabbits. 303 19

Oxygen free radicals have been implicated in the pathogenesis of postischemic liver injury. High-dose superoxide dismutase (SOD), a radical scavenging enzyme, has been investigated in a rat model of liver ischemia reperfusion by biochemical monitoring. Blood vessels to the median and left lobe were clamped for 1 h and then reperfusion was allowed. The indices used were serial venous blood levels of AST, ALT, calcium, and ATP determination in liver tissue. In SOD-treated animals (7,5000 U i.v.) a significant attenuation of the rise in enzyme levels was observed as well as the absence of the decrease in calcium level in the early phase after reperfusion as compared with control rats, and furthermore ATP restoration was significantly increased.
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PMID:Effect of superoxide dismutase on liver ischemia-reperfusion injury in the rat: a biochemical monitoring. 322 31

PAP of harvested livers is routinely used to minimize parenchymal anoxia during storage. PP is compared with PAP to evaluate the relative reliability of PAP. Sixty female Landrace pigs were used for 30 OLTs. Group 1 livers underwent PP, whereas group 2 livers were treated with PAP. The cold ischemic time was less than 120 minutes for both groups, with no warm ischemia. Intraoperative and 24-hour postoperative biochemical, coagulation, and histocytological data were analyzed. Morphological studies of cellular damage were based on the percentage of CVD and KP and classified as light, moderate, and severe damage. Data, at closing, were compared by using Fisher's test (group 1 v group 2,P = 0.003 for light damage and P = .04 for severe damage; first postoperative day for group 1 v group 2, P = .133 for light damage and P = .25 for severe damage. Blood samples at closing and 24 hours postoperatively showed significant differences between groups 1 and 2: At closing for groups 1 and 2, respectively: AST, 968.9 +/- 742.7 and 327.4 +/- 174.7 IU/L (P less than .001); ALT, 63.1 +/- 40.3 and 20.3 +/- 5.3 IU/L (P less than .001); AP, 292.2 +/- 107.1 and 139.5 +/- 45.3 IU/L (P less than .001); and 24 hours postoperatively for groups 1 and 2, respectively: AST, 1,664.9 +/- 917.8 and 419.3 +/- 230.9 IU/L (P less than .001): ALT. 180.4 +/- 28.9 and 66.4 +/- 17.5 IU/L (P less than .001); AP, 602.1 +/- 153.3 and 255.7 +/- 116.3 IU/L (P less than .01). Comprehensively, the results reflect a better perfusate distribution of the PAP livers compared with PP ones: uniform organ preservation, faster metabolic recovery, and reduced postoperative mortality.
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PMID:Comparison of combined portal-arterial versus portal perfusion during liver procurement. 327 50

Hepatic function was assessed by the aminopyrine breath test (ABT) in male Sprague Dawley rats 24 h after partial hepatic ischemia. ABT decreased progressively to 26.3 (p less than 0.05) and 19.7% of dose (p less than 0.05) after 90 and 120 min of ischemia, respectively. ABT at 24 h after injury was correlated to the concentration of ATP in the ischemic lobes 1 h after the onset of reperfusion (r2 = 0.971) but not to ALT activity in plasma at 1 h (r2 = 0.391). We conclude that postischemic ATP levels are a better index of subsequent hepatic function than ALT.
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PMID:Postischemic ATP levels predict hepatic function 24 hours following ischemia in the rat. 337 51

Oxygen-derived free radicals might play a role in the injury produced by reperfusion of ischemic organs. Since the generation of reactive oxygen species results in an increased formation of glutathione disulfide, we have attempted to document an oxidant stress during reperfusion of ischemic liver by following the hepatic production of glutathione disulfide in vivo and in the perfused rat liver. Following partial hepatic ischemia of 120 min duration, the plasma concentration of glutathione disulfide gradually increased from 0.8 +/- 0.1 to 9.1 +/- 1.6 microM (mean +/- S.E., n = 6) after 1 hr of reperfusion. The plasma concentration of reduced glutathione increased only 2-fold from 21.4 +/- 2.4 to 38.1 +/- 3.4 microM. The rise in plasma glutathione disulfide was higher with increasing duration of ischemia from 30 to 120 min and was associated with a gradual increase in hepatic glutathione disulfide. The hepatic origin of glutathione disulfide was documented in the perfused rat liver where the release of glutathione disulfide increased gradually during reperfusion following 90 min of warm ischemia from 1.0 +/- 0.1 to 2.6 +/- 0.5 nmole per min per gm liver at 30 min after onset of reperfusion. The administration of allopurinol, an inhibitor of xanthine oxidase, did not decrease the release of glutathione disulfide (29.9 +/- 3.8 nmoles per gm in controls vs. 44.7 +/- 10.0 nmoles per gm in 30 min with allopurinol) and ALT (3.3 +/- 1.4 units per gm in controls vs. 2.6 +/- 0.8 units per gm in 30 min with allopurinol). Our studies document an oxidant stress associated with reperfusion of ischemic liver.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Oxidant stress during reperfusion of ischemic liver: no evidence for a role of xanthine oxidase. 337 74

The effects of total ischemia and subsequent reperfusion on the formation of anaerobic metabolism products and their release into myocardial effluent were studied in isolated guinea pig hearts. During 30-min ischemia myocardial ATP and phosphocreatine decreased to 34 and 15% of the initial levels, respectively; this was accompanied by alanine formation and approximately stoichiometric glutamate loss. The increase in malate in ischemic myocardium corresponded to the anaplerotic flux aspartate----oxaloacetate----malate; the succinate production being commensurable to alpha-ketoglutarate formation in the alanine aminotransferase reaction. The release of lactate, alanine, succinate, creatine and pyruvate trace amounts into the myocardial effluent was observed during an early phase of the reperfusion using 1H-NMR. The rates of metabolite release reduced as follows: lactate much greater than alanine greater than succinate greater than creatine. By the 30th min of the reperfusion the decrease in these metabolites tissue contents was accompanied by the recovery of ATP and phosphocreatine levels up to 65 and 90% of the initial ones, respectively. The data obtained demonstrate that the formation and the release of succinate, alanine and creatine from the heart as well as of lactate may indicate profound disturbances in energy metabolism.
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PMID:An assessment of anaerobic metabolism during ischemia and reperfusion in isolated guinea pig heart. 337 59

The effect of ischemia on the formation of products of anaerobic metabolism and their release into the cardiac effluent in isolated perfused guinea pig hearts was studied. During 30 min normothermal ischemia, the myocardial ATP and phosphocreatine levels decreased to 34% and 15% of the initial values, respectively. The net alanine formation in ischemia was approximately a stoichiometric glutamate decrease; the increase in the tissue malate content corresponded to the aspartate----oxaloacetate----malate anaplerotic flux, the succinate production being commensurable to alpha-ketoglutaric acid formation in the alanine aminotransferase reaction. Using 1H-NMR, it was shown that the release of trace amounts of lactate, alanine, succinate, creatine and pyruvate into cardiac effluents occurred during the first 5 minutes of reperfusion. The rate of metabolite release decreased in the following order: lactate much greater than alanine greater than succinate greater than creatine. By the 30th minute of reperfusion, the decrease in the tissue levels of these metabolites to preischemic values was accompanied by the recovery of ATP and phosphocreatine to 65% and 90% of the initial levels, respectively. The data obtained suggest that the formation and release of alanine, creatine or succinate as well as lactate from ischemic myocardium may testify to significant disturbances in energy metabolism of the myocardium.
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PMID:[Formation of products of anaerobic metabolism in the ischemic myocardium]. 337 64

The biochemical characterization of experimental acute pancreatitis was performed by determination of the secretory enzymes lipase and alpha-amylase, of the cytoplasmic ALAT (alanine aminotransferase), of total protein and calcium concentration in serum of rats. The moderate and protracted course of the pathological process in the small animal model presented allowed to study the initial phase from 1-24 h. In the first 4-8 h most massive enzyme release into the intravasal space was observed. The level of enzyme activities was correlating with the severity of assault. One noxa alone (ischemia or juice edema) resulted in a moderate enzyme release (lipase : 2-2.5 fold of control). The action of both noxae caused a drastical increase in enzyme activities in the initial phase lipase : 8-20 fold, ALAT: 7 fold, alpha-Amylase: 2.5 fold). 24 h postoperatively the serum enzyme activities were at distinct pathological level. At this time acute pancreatitis provoked already a decreased serum protein content. A hypocalcemia was not observed.
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PMID:Contribution of pancreatic edema and short-term ischemia to experimental acute pancreatitis in the rat. II. Behaviour of serum parameters. 349 93

In order to investigate the applicability of liver transplantation after warm ischemia, a partial auxiliary auto-transplantation of the liver after 30 min of warm ischemia was carried out in 9 mongrel dogs. Among them, 6 dogs survived longer than 7 days. Liver functions, blood coagulability and histological changes were investigated before and after the transplantation. Serum GOT, LDH, and GPT levels were elevated immediately after transplantation, and returned to normal within a few days. Hemostatic tests also showed significant abnormalities after transplantation. Although PT and thrombotest became normal within a week, PTT and antithrombin III remained slightly abnormal for longer periods. Microscopically, vacuolization and degeneration of hepatocytes were observed after transplantation but they recovered completely within 4 weeks. Based on these results, it could be said that the livers subjected to warm ischemia for 30 min ischemia were still acceptable for auxiliary transplantation.
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PMID:Liver transplantation in dogs after 30 minutes of warm ischemia. 351 52


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