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)

The effect of low-dose dopamine administration on intramucosal pH (pHi) of the sigmoid colon and on postoperative function of various organs in patients undergoing elective abdominal aortic aneurysm repair was examined. Nineteen patients were randomized to two groups; nine received dopamine at a rate of 3 micrograms per kg per min for 24 h from induction of anaesthesia and ten control patients received fluids without dopamine. pHi was measured with a silicone tonometer and daily samples of blood were taken for measurement of liver transaminase activity, arterial oxygen saturation and creatinine concentration. Mean(s.e.m.) pHi fell to a significantly lower minimum value in those receiving dopamine compared with control patients (6.86(0.10) versus 7.11(0.08), P < 0.05). Five of the nine patients given dopamine developed intramucosal acidosis compared with only one of the ten control patients (P = 0.06). After operation the mean(s.e.m.) aspartate transaminase concentration in patients given dopamine rose from 33(2) to 80(17) units/l (P < 0.01); in control patients it rose from 32(3) to 59(16) units/l (P = 0.054). No differences between the groups was observed in the postoperative ratio of arterial oxygen saturation to inspired oxygen fraction or creatinine concentrations. These results indicate that dopamine has no beneficial effect on bowel mucosal oxygenation and function of the various organs in patients undergoing aortic aneurysm repair.
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PMID:Effect of low-dose dopamine on sigmoid colonic intramucosal pH in patients undergoing elective abdominal aortic aneurysm repair. 764 6

This study describes the carioprotective effect of ceruloplasmin (CAS 9031-37-2) against oxygen free radical injury, as indicated by several biochemical indicators and some cardiodynamic variables. Isolated rat hearts (n = 4-8, p < 0.05, for each experimental point) in Langendorff preparation were exposed to oxygen free radicals generated by electrolysis (10 mA) in the absence and the presence of 0.25 mumol/l purified ceruloplasmin and denaturated ceruloplasmin, in Krebs-Henseleit perfusion solutions. Biochemical indicators (noradrenaline, malondialdehyde, creatine-kinase, lactate dehydrogenase, aspartate aminotransferase, Ca2+ and Mg2+) as well as the electrocardiogram and the left ventricular pressure (LVP), were altered by oxygen free radicals formation, denoting major cellular and tissular damages in the nontreated hearts. Ceruloplasmin exhibited a cardioprotective effect and prevented the oxygen free radical-induced release of noradrenaline, indicating that it can also protect the sympathetic nerve endings from oxygen free-radical injury. Purified ceruloplasmin, a circulating extracellular antioxidant and oxygen free radical scavenger, seems to be an effective heart protective agent against myocardial and neuronal injuries generated by oxygen free radicals.
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PMID:Protection of myocardial tissue against deleterious effects of oxygen free radicals by ceruloplasmin. 777 45

The effects of total intravenous anaesthesia with an intravenous infusion of a combination of guaiphenesin, ketamine and detomidine were studied in 10 patients scheduled for elective surgery. Anaesthesia was maintained by the infusion of guaiphenesin (100 mg/ml), ketamine (2 mg/ml) and detomidine (0.02 mg/ml). The infusion rate was 1 ml/kg/hr. During anaesthesia, pulse rate and mean arterial blood pressure were continuously recorded. Arterial blood gases and pH were determined immediately after induction and at stated times during anaesthesia. Venous blood was sampled to determine plasma glucose, lactate, lactate dehydrogenase (LDH), creatine phosphokinase (CPK) and aspartate aminotransferase (AST) concentrations. Values were compared with those determined in blood sampled before the premedication. All determined parameters with the exception of the plasma glucose concentration, the arterial oxygen tension and the AST concentration did not change significantly and remained within normal ranges. The plasma glucose concentration increased significantly after the induction of anaesthesia compared to the control value but decreased to normal values during anaesthesia. The arterial oxygen tension was on average 30% lower than normally wished. Compared to the control value the plasma concentration of AST was significantly decreased at the end of anaesthesia. Based upon the results of this study an infusion of guaiphenesin, ketamine and detomidine appears to be useful for the maintenance of total anaesthesia in horses.
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PMID:Intravenous anaesthesia in horses by guaiphenesin-ketamine-detomidine infusion: some effects. 780 4

Previous studies have demonstrated a role for both tumor necrosis factor (TNF) and reactive oxygen intermediates (ROI) in hepatic ischemia/reperfusion (I/R) injury. Biologically active TNF was present in liver homogenates in ischemic and nonischemic lobes after 2 h of ischemia but without reperfusion. Using an in situ liver perfusion model, we measured ROI, TNF, and hepatic enzymes in the effluent after 2 h of ischemia. Increased reduction of ferricytochrome C was observed in the hepatic effluent, indicative of the formation of ROI. Treatment of animals with TNF neutralizing antisera significantly reduced both ROI and aspartate aminotransferase (AST). Animals treated with superoxide dismutase (SOD), or SOD + catalase (CAT) had greater TNF in the hepatic effluent compared with I/R alone; however, SOD or SOD + CAT did not cause additional release of AST.SOD + CAT plus anti-TNF serum resulted in significant protection compared with SOD + CAT plus control serum. Reperfusion of ischemic liver with 4 mM H2O2 increased both TNF and AST. Optimal protection of hepatocellular injury from reperfusion injury is achieved with a combination of antioxidants and inhibition of TNF.
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PMID:Hepatic ischemia/reperfusion injury: importance of oxidant/tumor necrosis factor interactions. 781 Jun 59

Little is known about the kinetics of most serum enzymes during the first hours of life, and even less about the effect on such enzyme activities of perinatal hypoxia-ischaemia. It was the aim of the present study to evaluate the serum kinetics of seven differently located cell enzymes in healthy and asphyxiated newborns during the 1st week of life. The serum activities of cytoplasmic and mitochondrial [aspartate aminotransferase (ASAT), creatine kinase (CK), glutamate dehydrogenase (GLDH), lactate dehydrogenase (LDH), and hydroxybutyrate dehydrogenase (HBDH)] and membrane-bound (gamma-glutamyl-transferase and leucine arylaminidase) enzymes were prospectively measured in full-term asphyxiated (n = 49) and healthy (n = 87) newborns during the first 144 h of life. The blood samples were taken serially at five fixed times: 0 (cord), 12, 24, 72, and 144 h postpartum. The asphyxiated newborns had significantly increased serum activities of ASAT, LDH, and HBDH up to 72 h postpartum, whereas healthy newborns showed higher CK and GLDH activities. Only the activities of ASAT, LDH, and HBDH seemed to depend on the oxygen supply of the fetus or newborn. If other causes of increased serum enzyme activities, e.g. liver diseases, haemolytic disorders, tumours, or inborn errors of metabolism, are excluded, elevated serum activities of ASAT, LDH, and HBDH should draw one's attention to a perinatal hypoxic-ischaemic insult of the newborn.
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PMID:Serum enzyme activities in full-term asphyxiated and healthy newborns: enzyme kinetics during the first 144 hours of life. 791 42

In 30 patients undergoing elective repair of abdominal aortic aneurysm the intramucosal pH (pHi) of the sigmoid colon was measured. Blood for endotoxin assay was taken at intervals before, during and after surgery. Daily measurements were made of liver transaminase activity and of arterial partial pressure of oxygen (PaO2). The mean (s.e.m.) peak systemic endotoxin concentration in those who developed intramucosal acidosis (pHi below 7.00) was 90(14) pg/ml, compared with 42(5) pg/ml in those who did not (P < 0.01). In the 14 patients whose pHi fell below 7.00, the mean (s.e.m.) postoperative rise in aspartate transaminase activity was 346(74) per cent, compared with 181(20) per cent in those whose pHi remained above this level (P < 0.05). The mean (s.e.m.) postoperative ratio of PaO2 to the fraction of inspired oxygen was 177(11) mmHg in those with intramucosal acidosis, compared with 260(24) mmHg in those whose pHi remained above 7.00 (P < 0.01). These results demonstrate a relationship between bowel ischaemia, endotoxaemia and organ impairment following elective aneurysm repair.
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PMID:Bowel ischaemia and organ impairment in elective abdominal aortic aneurysm repair. 774 17

This study investigated the effect of verapamil on prolonged and severe ischemic injury and elucidated the association of the calcium blocking action with cellular injury, assessing changes in hepatic calcium concentrations during ischemia and reperfusion in pigs. Hepatic ischemia was produced for 180 min by clamping both the hepatic artery and portal vein during temporary portacaval shunt performed before the induction of ischemia. Pigs were divided into two groups: the animals in the verapamil group (Group V, n = 6) received continuous administration of 0.025 mg/kg per min of verapamil intraportally for 20 min before ischemia. The control group (Group C) received nothing. A better survival rate was observed in Group V than in Group C (p < 0.01), but serum aspartate aminotransferase was higher in Group V after reperfusion (p < 0.05). There were no significant changes in hepatic calcium concentrations during ischemia in either group, but it increased immediately after reperfusion in both groups. However, no significant difference was found between the two groups. Recovery of the pyruvate/lactate ratio in Group V tended to be better after reperfusion compared to Group C (p = 0.08). These data suggest that the pre-ischemic administration of verapamil produced better survival in animals after prolonged normothermic ischemia. However, the reperfused liver suffered more severe damage in the first 6 h after reperfusion in the verapamil-treated animals. Moreover, there seemed to be very little blocking action of calcium influx. A reduced oxygen requirement may be involved in the protective action of verapamil on animal survival.
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PMID:Effect of verapamil on hepatic reperfusion injury after prolonged ischemia in pigs. 798 12

Six healthy horses were anaesthetised with halothane (1.2 times the horse minimal alveolar concentration) in oxygen for more than 12 hours. Serum bilirubin, aspartate aminotransferase, alkaline phosphatase and L-iditol dehydrogenase values were significantly (P < 0.05) increased for up to nine days after anaesthesia. These changes suggest an anaesthesia related liver dysfunction. Creatine kinase increased to an average of more than 1400 IU litre-1 24 hours after anaesthesia and this change is indicative of muscle cell disruption. Renal-associated biochemical results, (that is serum creatinine and inorganic phosphate concentrations) were significantly increased transiently and are indicative of reduced renal function during and immediately after anaesthesia. Plasma concentrations of eicosanoids (6-keto-PGF1a, PGF2a, PGE and thromboxane) following anaesthesia were not different from preanaesthetic values. The magnitude of liver and muscle cell related increases in serum enzyme activities resulting from prolonged halothane anaesthesia was in excess of that previously reported for anaesthesia of shorter duration.
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PMID:Biochemical and haematological changes following prolonged halothane anaesthesia in horses. 828 98

Quinidine in vitro significantly reduced accumulation of TEA (tetraethyl ammonium) and PAH (p-amino hippurate) and inhibited oxygen consumption in renal cortical slices. Mitochondrial respiratory control index (RCI) and ADP/O ratio were decreased. Intraperitoneal administration of quinidine at 75 mg/kg twice a day for four days inhibited TEA transport in renal cortical slices and decreased oxygen consumption. Mitochondria showed a reduction in ADP/O ratio but no change in RCI. Serum biochemical measurements indicated a significant elevation in serum creatinine, alanine aminotransferase (ALT), and aspartate aminotransferase (AST).
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PMID:In vitro and in vivo effects of quinidine on the kidneys in Fischer-344 rats. 830 84

Reoxygenation of rat-liver mitochondria after anoxic incubation induced release of matrix proteins. As assessed by release of a matrix enzyme, it was proportional to the rate of H2O2 production. The release was not observed with low concentrations of extramitochondrial free Ca2+, indicating a Ca(2+)-dependent pathway. Phospholipase A2 was not involved in the reoxygenation injury, because non-esterified fatty acids did not increase on reoxygenation even when re-acylation was inhibited and because inhibitors of phospholipase A2 had little effect on enzyme release. Cyclosporin A, ATP, ADP and inhibitors of pyridine nucleotide oxidation had a protective effect, strongly suggesting involvement of so-called Ca(2+)-dependent permeability transition. Ca2+ was also released from reoxygenated mitochondria and inhibition of reuptake of released Ca2+ attenuated the enzyme release. Similar releases of aspartate aminotransferase and Ca2+ were observed with mitochondria in an oxygen radical-generating system, hypoxanthine and xanthine oxidase. In this system, lecithin-cardiolipin liposomes also released entrapped Ca2+ without disruption of the membrane. From these results, we conclude that during reoxygenation, Ca2+ release and subsequent reuptake induced permeability transition of mitochondria, resulting in reoxygenation injury.
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PMID:Ca(2+)-induced, phospholipase-independent injury during reoxygenation of anoxic mitochondria. 841 80


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