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)

Anaesthesia was induced in 24 horses with xylazine and ketamine and maintained with halothane (12 cases) or enflurane (12 cases) in oxygen. Pulse rate, arterial blood pressure, arterial blood gas values, respiratory rate and tidal volume were measured at regular intervals during anaesthesia. Serial venous blood samples were taken for assay of glucose, urea, haemoglobin, packed cell volume, gamma glutamyl transpeptidase, aspartate aminotransferase, alanine aminotransferase and creatine kinase. Operating conditions and the horses' behaviour in the recovery period were also recorded. In the case of the group of horses receiving enflurane, difficulty was experienced maintaining anaesthesia deep enough for surgery. This group also displayed greater respiratory depression. There were no significant differences between arterial blood pressure values, or any of the haematological or biochemical parameters recorded in each group. Recovery from anaesthesia was significantly faster in horses receiving enflurane but less smooth. It was concluded that, although enflurane appeared to be safe in the horse, the respiratory depression and the unpleasant recovery did not make it a desirable alternative to halothane.
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PMID:Clinical anaesthesia in the horse: comparison of enflurane and halothane. 397 74

Although liver perfusion in situ is a valuable technique for the study of hepatic metabolism, it has rarely been applied to the study of mice. This is primarily due to the lack of a simple, reproducible technique to cannulate the delicate portal vein and initiate perfusion without irreversible hepatic injury. Therefore, we developed a technique to overcome these obstacles and performed studies to assess the viability of the perfused murine liver. The inflow catheter assembly permits rapid, reproducible cannulation of the portal vein and protects the cannulated vein from the effects of subsequent manipulations. Serial assessments of perfusion pressure, flow rate, perfusate pH, oxygen consumption, and fluxes of alanine aminotransferase and potassium indicate that the murine liver remains viable during perfusion. Moreover, the light and electron microscopic appearance of perfused livers is indistinguishable from that of freshly excised control livers. This technique should facilitate perfusion studies of hepatic metabolism in murine strains with genetic homogeneity and defined genetic abnormalities of hepatic metabolism.
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PMID:Isolated perfusion of murine liver in situ: technique and validation. 408 53

A case of subarachnoid hemorrhage complicated by neurogenic pulmonary edema and neurogenic myocardial damage is reported. A 50-year-old woman was admitted following the sudden onset of headache and disturbance of consciousness due to a ruptured internal carotid posterior communicating artery aneurysm on the right side. She showed respiratory failure due to pulmonary edema, which subsequently improved with the mechanical ventilation. After that, she manifested chest distress and hypotensive episode then occurred. An ECG showed QS wave and ST elevation which suggested the presence of inferolateral myocardial damage. Subsequent rises in serum GOT, GPT, LDH and CPK were noticed. CPK-MB and LDH I and V isozyme levels rose. An echo cardiogram showed hypokinesis of the apical half of the left ventricular septum. The patient died on 5th hospital day due to rerupture of the cerebral aneurysm. Autopsy revealed diffuse myocytolysis with coagulation necrosis of the heart muscle without occlusion of coronary arteries. A small hemorrhagic lesion was found in the hypothalamus. We suggested that a hypothalamic lesion due to subarachnoid hemorrhage stimulated the sympathetic nervous system which in turn discharged endogenic catecholamine. This was probably accompanied by vasospasm of the coronary arteries and systemic peripheral arterioles. Furthermore, myocardial oxygen consumption could have been increased by the increase in catecholamine. Finally, it gave rise to neurogenic pulmonary edema and extensive diffuse myocytolysis of the heart occurred.
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PMID:[Myocardial damage (myocytolysis) caused by subarachnoid hemorrhage]. 409 85

1. A method is described for extracting separately mitochondrial and extramitochondrial enzymes from fat-cells prepared by collagenase digestion from rat epididymal fat-pads. The following distribution of enzymes has been observed (with the total activities of the enzymes as units/mg of fat-cell DNA at 25 degrees C given in parenthesis). Exclusively mitochondrial enzymes: glutamate dehydrogenase (1.8), NAD-isocitrate dehydrogenase (0.5), citrate synthase (5.2), pyruvate carboxylase (3.0); exclusively extramitochondrial enzymes: glucose 6-phosphate dehydrogenase (5.8), 6-phosphogluconate dehydrogenase (5.2), NADP-malate dehydrogenase (11.0), ATP-citrate lyase (5.1); enzymes present in both mitochondrial and extramitochondrial compartments: NADP-isocitrate dehydrogenase (3.7), NAD-malate dehydrogenase (330), aconitate hydratase (1.1), carnitine acetyltransferase (0.4), acetyl-CoA synthetase (1.0), aspartate aminotransferase (1.7), alanine aminotransferase (6.1). The mean DNA content of eight preparations of fat-cells was 109mug/g dry weight of cells. 2. Mitochondria showing respiratory control ratios of 3-6 with pyruvate, about 3 with succinate and P/O ratios of approaching 3 and 2 respectively have been isolated from fat-cells. From studies of rates of oxygen uptake and of swelling in iso-osmotic solutions of ammonium salts, it is concluded that fat-cell mitochondria are permeable to the monocarboxylic acids, pyruvate and acetate; that in the presence of phosphate they are permeable to malate and succinate and to a lesser extent oxaloacetate but not fumarate; and that in the presence of both malate and phosphate they are permeable to citrate, isocitrate and 2-oxoglutarate. In addition, isolated fat-cell mitochondria have been found to oxidize acetyl l-carnitine and, slowly, l-glycerol 3-phosphate. 3. It is concluded that the major means of transport of acetyl units into the cytoplasm for fatty acid synthesis is as citrate. Extensive transport as glutamate, 2-oxoglutarate and isocitrate, as acetate and as acetyl l-carnitine appears to be ruled out by the low activities of mitochondrial aconitate hydratase, mitochondrial acetyl-CoA hydrolyase and carnitine acetyltransferase respectively. Pathways whereby oxaloacetate generated in the cytoplasm during fatty acid synthesis by ATP-citrate lyase may be returned to mitochondria for further citrate synthesis are discussed. 4. It is also concluded that fat-cells contain pathways that will allow the excess of reducing power formed in the cytoplasm when adipose tissue is incubated in glucose and insulin to be transferred to mitochondria as l-glycerol 3-phosphate or malate. When adipose tissue is incubated in pyruvate alone, reducing power for fatty acid, l-glycerol 3-phosphate and lactate formation may be transferred to the cytoplasm as citrate and malate.
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PMID:The intracellular localization of enzymes in white-adipose-tissue fat-cells and permeability properties of fat-cell mitochondria. Transfer of acetyl units and reducing power between mitochondria and cytoplasm. 439 82

1. Transient and steady-state changes caused by acetate utilization were studied in perfused rat heart. The transient period occupied 6min and steady-state changes were followed in a further 6min of perfusion. 2. In control perfusions glucose oxidation accounted for 75% of oxygen utilization; the remaining 25% was assumed to represent oxidation of glyceride fatty acids. With acetate in the steady state, acetate oxidation accounted for 80% of oxygen utilization, which increased by 20%; glucose oxidation was almost totally suppressed. The rate of tricarboxylate-cycle turnover increased by 67% with acetate perfusion. The net yield of ATP in the steady state was not altered by acetate. 3. Acetate oxidation increased muscle concentrations of acetyl-CoA, citrate, isocitrate, 2-oxoglutarate, glutamate, alanine, AMP and glucose 6-phosphate, and lowered those of CoA and aspartate; the concentrations of pyruvate, ATP and ADP showed no detectable change. The times for maximum changes were 1min, acetyl-CoA, CoA, alanine and AMP; 6min, citrate, isocitrate, glutamate and aspartate; 2-4min, 2-oxoglutarate. Malate concentration fell in the first minute and rose to a value somewhat greater than in the control by 6min. There was a transient and rapid rise in glucose 6-phosphate concentration in the first minute superimposed on the slower rise over 6min. 4. Acetate perfusion decreased the output of lactate, the muscle concentration of lactate and the [lactate]/[pyruvate] ratio in perfusion medium and muscle in the first minute; these returned to control values by 6min. 5. During the first minute acetate decreased oxygen consumption and lowered the net yield of ATP by 30% without any significant change in muscle ATP or ADP concentrations. 6. The specific radioactivities of cycle metabolites were measured during and after a 1min pulse of [1-(14)C]acetate delivered in the first and twelfth minutes of acetate perfusion. A model based on the known flow rates and concentrations of cycle metabolites was analysed by computer simulation. The model, which assumed single pools of cycle metabolites, fitted the data well with the inclusion of an isotope-exchange reaction between isocitrate and 2-oxoglutarate+bicarbonate. The exchange was verified by perfusions with [(14)C]bicarbonate. There was no evidence for isotope exchange between citrate and acetyl-CoA or between 2-oxoglutarate and malate. There was rapid isotope equilibration between 2-oxoglutarate and glutamate, but relatively poor isotope equilibration between malate and aspartate. 7. It is concluded that the citrate synthase reaction is displaced from equilibrium in rat heart, that isocitrate dehydrogenase and aconitate hydratase may approximate to equilibrium, that alanine aminotransferase is close to equilibrium, but that aspartate transamination is slow for reasons that have yet to be investigated. 8. The slow rise in citrate concentration as compared with the rapid rise in that of acetyl-CoA is attributed to the slow generation of oxaloacetate by aspartate aminotransferase. 9. It is proposed that the tricarboxylate cycle may operate as two spans: acetyl-CoA-->2-oxoglutarate, controlled by citrate synthase, and 2-oxoglutarate-->oxaloacetate, controlled by 2-oxoglutarate dehydrogenase; a scheme for cycle control during acetate oxidation is outlined. The initiating factors are considered to be changes in acetyl-CoA, CoA and AMP concentrations brought about by acetyl-CoA synthetase. 10. Evidence is presented for a transient inhibition of phosphofructokinase during the first minute of acetate perfusion that was not due to a rise in whole-tissue citrate concentration. The probable importance of metabolite compartmentation is stressed.
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PMID:Control of the tricarboxylate cycle and its interactions with glycolysis during acetate utilization in rat heart. 544 22

In 38 patients subjected to retropubic prostatectomy the effects of continuous lumbar epidural analgesia for 24 hours and the thiopentone- oxygen-nitrous oxide- alcuronium-pethidine sequence with artificial ventilation on the serum activities of aspartate aminotransferase (ASAT), alanine aminotransferase (ALAT), alpha-hydroxybutyrate dehydrogenase (HBD), and alkaline phosphatase (AP) have been studied. Per- and postoperative complications were recorded according to a prearranged plan designed to quantify the peroperative haemorrhage, postoperative deep vein thrombosis, pulmonary, circulatory and infectious complications. ASAT, ALAT and AP in the general group and ALAT in the epidural group showed significant increases on the 5th and 7th postoperative days. There existed no statistically significant difference between the groups. 82% of the patients with documented postoperative complications combined with hypoxaemia showed a pathologic liver enzyme pattern in contrast to 9% of the patients with uneventful postoperative course. It is concluded that the method of anaesthesia did not have an effect on the liver enzymes. Complications combined with postoperative hypoxaemia seemed to be the factors responsible for the increases of liver enzymes.
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PMID:Liver enzymes after retropubic prostatectomy in patients receiving continuous lumbar epidural analgesia or general anaesthesia. 618 33

Burn injury is associated with an elevation in total body oxygen consumption, increased hepatic alanine uptake and conversion to glucose, and a negative nitrogen balance. The primary source of the alanine used for gluconeogenesis by the liver and of the nitrogen lost as urea is believed to be from skeletal muscle. Selected muscle regulatory enzymes and pyruvate and oleate oxidation rates were assayed for maximal activity during the postburn period. Male Sprague-Dawley rats that received 50% total body surface scald burns on the dorsum and abdomen were examined for citrate synthase (CS), phosphofructokinase (PFK), and glutamate-pyruvate transaminase (GPT) activity in uninjured muscle at 3, 7, 13, and 20 days postburn, and the ability of muscle to oxidize pyruvate and oleate was measured at 3 and 13 days after injury. Cs, PFK, and GPT activities increased significantly (p less than 0.05) by 13-20 days after injury in the soleus and diaphragm. The epitrochlearis showed no change in CS, but PFK and GPT were elevated within this time frame. The gastrocnemius muscle showed an elevated oleate oxidation rate at 13 days after injury, but no change at 3 days postburn. Pyruvate oxidation rates were unaltered. The results of this study indicate that during the postburn period several metabolic alterations occur in muscle. These adaptations include: (1) elevated CS activity which may be associated with increased oxidative capacity,, (2) increased PFK activity which implies that more substrate is being shuttled through the glycolytic pathway, (3) increased GPT activity which may reflect increased pyruvate conversion to alanine, and (4) increased oleate oxidation rates which demonstrate that muscle is utilizing more fatty acid substrates during the postburn period.
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PMID:Altered muscle metabolism in rats after thermal injury. 621 91

Hyperbaric oxygen (HPO) was administered to rats (100% O2 at 2.8 atm for 90 min) immediately or 1 hr after severe carbon tetrachloride (CCl4) intoxication in order to study the mechanisms of protection against hepatocellular injury by hyperoxia. Slight to moderate hepatocellular injury was observed, particularly by morphologic criteria, 4 hr after CCl4 intoxication. Little cell death was observed; 24 hr after CCl4, 20% of the untreated animals died. In the survivors, the following typical changes occurred in the liver: extensive hepatocellular swelling, vacuolization and necrosis; severe ultrastructural alterations; binding of CCl4 to microsomal lipids; elevation of lipid peroxidation products (conjugated dienes); little decrease in cytochrome b5 and severe decrease in cytochrome P-450 levels. Serum transaminase (alanine aminotransferase and aspartate aminotransferase) levels were elevated. Immediate treatment with HPO prevented the mortality and markedly decreased the hepatocellular necrosis 24 hr after intoxication. Immediate HPO treatment did not lower the levels of free CCl4 in the liver. However, the rise in lipid peroxidation products caused by CCl4 intoxication at 4 hr was reduced. Delayed treatment with HPO (1 hr after CCl4) prevented the mortality but was less effective in preventing necrosis. Some hepatocellular protection was still demonstrable. In particular, the rise in lipid peroxidation products was reduced. Hyperoxia protects hepatocytes against CCl4 toxicity. The rapid decline in protective effect within 60 min of intoxication suggests that hyperoxia inhibits CCl4 activation and/or damage from molecular intermediates. Hyperoxia has little effect on the progression of sublethal injury to cell death in the livers of CCl4-intoxicated rats.
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PMID:Protection of hepatocytes with hyperoxia against carbon tetrachloride-induced injury. 653 53

Effects of corticosteroids and surgical stress on hepatic morphologic features and enzymes were studied in 18 mature dogs of mixed breeding: group 1, control (n = 3); group 2, dexamethasone (n = 5); group 3, dexamethasone and surgery (n = 5); and group 4, surgery (n = 5). Dexamethasone (2.2 mg/kg of body weight twice a day subcutaneously) was administered for 8 days in groups 2 and 3 dogs. All dogs were anesthetized with thiopental for 10 minutes on days 0, 2, and 4. On day 2, dogs in groups 3 and 4 were intubated and maintained on methoxyflurane and oxygen, and a liver biopsy, hemilaminectomy (T13-L1), and 15 minutes of hypotension (75/45 mm of Hg) induced by methoxyflurane were done. Serum alkaline phosphatase (ALP) activity, ALP isoenzymes, and alanine aminotransferase (ALT) activity were determined on days 0, 2, 3, 5, and 8. All dogs were euthanatized and necropsied on day 8. Serum hepatic enzyme activity and hepatic morphologic characteristics were normal for group 1 control dogs. The mean ALP and ALT were significantly (P less than 0.05) increased in dogs in groups 2, 3, and 4. In group 2, the mean ALP (days 5 to 8) and ALT (day 8) were significantly (P less than 0.05) increased. In group 3, the mean ALP and ALT activities were significantly increased on days 2 to 8. In group 4, the mean ALP was significantly increased on days 2 to 8 and the mean ALT was significantly increased on days 3 and 5. All other values were normal. A single isoenzyme band (Rf = 0.399 +/- 0.023, mean +/- SD) was identified in all dogs. Hepatic morphologic changes attributed to dexamethasone were mild-to-moderate vacuolation in a diffuse distribution on day 2 (group 3) and aggregates of moderate-to-severe vacuolation in mainly a periportal distribution on day 8 (groups 2 and 3).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of dexamethasone and surgical hypotension on hepatic morphologic features and enzymes of dogs. 665 Sep 53

A training program was started in nine patients with chronic active hepatitis in clinical remission while receiving immunosuppressive therapy. The patients were examined before and after a training period of 4-5 weeks and 10-12 weeks, respectively. The calculated oxygen consumption increased by 19% and 29%, and the estimated work load capacity improved. No change occurred in alanine aminotransferase, aspartate aminotransferase, alkaline phosphatases, gamma-glutamyl-transpeptidase, serum bilirubin, or prealbumin, whereas creatine kinase and lactate dehydrogenase increased significantly. The clinical condition did not worsen in any patient, and most of the patients felt that their physical performance capacity had improved. We conclude that long-term regular physical training is well tolerated by patients with chronic active hepatitis in clinical remission and that training leads to improvement in the oxygen consumption and the estimated work load capacity in such patients.
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PMID:Improvement of physical capacity after long-term training in patients with chronic active hepatitis. 667 79


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