Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P17174 (aspartate aminotransferase)
 14,872 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serial physiological responses were examined for 150 min from captive collared peccaries during immobilization with ketamine hydrochloride. Rectal temperatures decreased significantly (P less than 0.01) during anesthesia. Serum concentrations of total proteins, albumin, cholesterol, alanine aminotransferase, and calcium declined significantly (P less than 0.05) during the first 45 min post-immobilization before stabilizing. Concentrations of lactate dehydrogenase and alkaline phosphatase in sera showed similar but nonsignificant (P greater than 0.05) trends. Inorganic phosphorus and aspartate aminotransferase concentrations increased significantly (P less than 0.05) throughout the trial. Concentrations of serum glucose and glucocorticoid during the immobilization period were highly variable between individuals. Serum electrolytes, urea nitrogen, creatinine, gammaglutamyl transferase and progesterone were not significantly (P greater than 0.05) affected by immobilization. Elevations in serum testosterone were noted. Results indicated appropriate sampling times relative to immobilization for assay of particular serum biochemicals and steroid hormones during investigations of the physiology of the collared peccary.
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PMID:Endocrine and metabolic responses of the collared peccary (Tayassu tajacu) to immobilization with ketamine hydrochloride. 300 72

Hypoxia, phenobarbital induction, and halothane anesthesia have been implicated in the pathogenesis of hepatotoxicity in the rat model. However, a controversy exists over the role of halothane in liver injury; does it act by reducing hepatic blood flow, thereby inducing hypoxia, or do its metabolites initiate the injury? These variables are difficult to separate during in vivo halothane exposure. In the present experiments, effects of halothane on hepatic perfusion were eliminated by exposing confluent monolayers of hepatocytes isolated from Fisher 344 rats livers, both with and without phenobarbital pretreatment, to 1.5% halothane or 2.0% isoflurane in 1%, 2%, or 4% (control) oxygen. Isoflurane exposure was included for a control of anesthetic effects on hepatocytes, because it is known to be metabolized minimally and probably is not associated with hepatic dysfunction. Oxygen levels were chosen to approximate those that may occur in the liver in vivo. Cell death was assayed via aspartate aminotransferase (AST) release, both immediately following a 2-h oxygen +/- anesthetic exposure and 6 h post-exposure. Per cent cell death data were analyzed using multiple regression techniques. Results obtained immediately, and 6 h after, exposure demonstrate that low oxygen levels, halothane, and phenobarbital were each highly significant factors (P less than .001) in relation to cell death, in agreement with the halothane-phenobarbital-hypoxia rat model. A toxic effect of isoflurane was not observed under identical experimental conditions. The results of the study clearly indicate that the origin of cell death in hepatocyte monolayers is multi-factorial; hypoxia, phenobarbital induction, and halothane exposure each contribute to the hepatocyte damage observed in our in vitro model.
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PMID:Comparative toxicity of halothane, isoflurane, hypoxia, and phenobarbital induction in monolayer cultures of rat hepatocytes. 335 86

The toxicity of several halogenated and non-halogenated hydrocarbons (CH2Cl2, CHCl3, CCl4, C6H14, C8H10) in isolated rat hepatocytes were compared. Release of aspartate aminotransferase (AST) activity was rapid and concentration-dependent. Fractional AST release plateaued at 10-60 min following hydrocarbon exposure. Enzyme leakage at 60 min correlated with the oil/water partition coefficient (pi) of the compounds. All compounds, except n-hexane, also caused an immediate inhibition of the rate of cellular respiration. Inhibition of cell respiration also correlated with pi and was reversible. The recovery of cellular oxygen consumption was examined in detail for CCl4 and correlated with evaporation of the compound. These data suggest that acute hydrocarbon-induced injury in isolated hepatocytes is mediated by concentration-dependent direct solvent effects. Since halogenated hydrocarbons are widely used to induce general anesthesia, the clinical implications of possible direct effects by halocarbons on liver function in vivo and the potential relationship to liver injury are discussed.
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PMID:Rapid halogenated hydrocarbon toxicity in isolated hepatocytes is mediated by direct solvent effects. 362 14

One goat anesthetized with thiamylal sodium, xylazine, and halothane for repair of an abominal hernia, and 7 of 29 goats similarly anesthetized for an experiment unrelated to considerations of anesthesia, developed signs of hepatic failure within 24 hours of anesthesia. Affected goats had high values for serum aspartate transaminase and serum total bilirubin by 12 to 24 hours after induction of anesthesia. Necropsy of the 8 affected goats revealed centrilobular to massive hepatic necrosis (8 of 8), brain lesions consistent with hepatic encephalopathy (3 of 4), and acute renal tubular necrosis (6 of 6). Two unaffected goats had no hepatic necrosis. Causes of hepatic necrosis other than those related to anesthesia (eg, infectious agents, toxins) were ruled out by lack of supporting necropsy findings or were considered unlikely because of lack of opportunity for exposure. Hepatic lesions in these goats closely resembled those described in human beings with halothane-associated hepatic injury, although in both species these lesions are nonspecific at the gross and light microscopic levels. The pathogenesis of halothane-associated hepatic injury in goats, as in human beings, remains to be determined.
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PMID:Hepatic necrosis following halothane anesthesia in goats. 379 99

The effect of halothane-induced hypotension on the development of postanesthetic myopathy was studied, using 6 healthy adult horses. Horses were anesthetized with halothane in oxygen for 3.5 hours on each of 2 occasions. Intermittent positive-pressure ventilation was used to maintain PaCO2 of 45 to 55 mm of Hg throughout both anesthetic exposures. By regulating the inspired halothane concentration, a mean arterial blood pressure of 85 to 95 mm of Hg (normotension) was maintained throughout the 1st anesthetic exposure, and a mean arterial blood pressure of 55 to 65 mm of Hg (hypotension) was maintained during the 2nd anesthetic exposure. All horses recovered uneventfully from normotensive anesthesia, but all had some muscle dysfunction after prolonged hypotensive anesthesia. Because of apparent animal discomfort and lameness involving more than 1 limb, 3 horses were euthanatized soon after they recovered from hypotensive anesthesia. The 3 other horses showed a degree of lameness. In addition, 1 horse had raised, swollen plaques over the hip, rib, and facial areas which were in contact with the surgical table, and another had evidence of facial nerve paralysis. One hour after the 6 horses stood after hypotensive anesthesia was completed, values obtained for aspartate transaminase and creatinine were significantly (P less than 0.05) greater than those obtained after normotensive anesthesia was completed. Aspartate transaminase, total bilirubin, and creatinine values were significantly (P less than 0.05) increased when compared with those obtained before horses were anesthetized. A large increase was measured in creatine kinase. Twenty-four hours after hypotensive anesthesia was completed, creatine kinase and lactate dehydrogenase in the 3 surviving horses were significantly (P less than 0.05) greater than those values after normotensive anesthesia was completed.
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PMID:Arterial hypotension and the development of postanesthetic myopathy in halothane-anesthetized horses. 382 55

Changes in three recognized liver function tests are reported following the use of propofol in 30 fit, unpremedicated women in whom propofol was used as the main anaesthetic agent. Doses of 140 to 330 mg were given, together with nitrous oxide and oxygen. All patients were undergoing minor gynaecological operations and all conformed to Grade 1 physical status of American Society of Anesthesiologists Classification. In none of these patients was there hypoxia or hypercarbia at any time during or following anaesthesia and none of the patients received any other drugs until completion of the study. No significant changes in liver enzymes (aspartate transaminase and alanine transaminase) or in serum alkaline phosphatase were detected.
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PMID:Changes in liver function tests after propofol ('Diprivan'). 387 86

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

Effects of yohimbine on xylazine-pentobarbital anesthesia were evaluated in ponies. Five minutes after the IV injection of xylazine (1.1 mg/kg of body weight), pentobarbital sodium (12.7 mg/kg, IV) and additional xylazine (2.2 mg/kg, IM) were given and produced anesthesia in 12 ponies for 64.0 +/- 16.4 minutes (mean +/- SD) as well as immobilization for 89.8 +/- 34.2 minutes. Eleven ponies were given yohimbine (0.1 mg/kg, IV) 50 minutes after pentobarbital dosing. In these 11 ponies, durations of anesthesia and immobilization were shorter, 52.0 +/- 1.4 and 65.5 +/- 14.8 minutes, respectively. The xylazine-pentobarbital combination caused bradycardia that was reversed by yohimbine injection. Xylazine-pentobarbital produced a small, but steady, decrease of mean arterial blood pressure, which was compounded by yohimbine administration and was evident for approximately 2 minutes. Within a minute after yohimbine injection, the ponies' respiratory rate decreased and the length of inspiration and expiration and thoracic breathing increased. This lasted approximately 2 to 3 minutes and was followed by an increase in respiratory rate. The anesthesia also produced a decrease in PaO2 that gradually returned to base line in 12 control ponies, but was more pronounced in 11 ponies given yohimbine. The PaCO2, although remaining moderately high in control ponies, returned to base line after yohimbine injection. An increased pHa was seen 60 minutes after induction of anesthesia and was especially noticeable after yohimbine administration. Decreases in the number of WBC, hemoglobin content, PCV, plasma protein and serum aspartate transaminase resulting from xylazine-pentobarbital were reversed by yohimbine. Conversely, serum glucose values and creatine kinase activities were increased by xylazine-pentobarbital.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antagonism of xylazine-pentobarbital anesthesia by yohimbine in ponies. 402 6

One hundred and forty-one randomly selected surgical patients, aged 35 years or over, were studied preoperatively, followed through their operative procedures, and reassessed during the first post-operative week for evidence of myocardial ischaemia associated with surgical operations under general anaesthesia. Of these patients 38% were found to have preoperative clinical evidence of heart disease, hypertension, or diabetes; 45% had abnormal preoperative E.C.G. patterns.Three patients experienced myocardial infarction during or within 36 hours of operation, all of the occult type; all were in the preoperative abnormal groups. Non-specific postoperative E.C.G. changes were equally common in the groups of patients with normal or abnormal preoperative electrocardiograms.A relationship existed between a rise in serum lactic dehydrogenase (L.D.H.) concentration and the field of the operation, but the diagnosis of infarction was not confused provided serum L.D.H. isoenzyme patterns and a rise in serum aspartate aminotransferase (S.G.O.T.) levels were consistent with the diagnosis.
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PMID:Myocardial infarction following surgical operations. 572 23

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


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