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)

In this study, we tested a new artificial liver device using liver pieces in 8-h hemoperfusion of comatous porcine blood and compared two alternative tissue preparations. Acute hepatic coma in the pigs was induced by complete devascularization of the liver. The animals were killed in stage IV coma (15-25 h after the operation), and 1 l blood was perfused over 200 g fresh or DMSO-preserved liver cubes. After the devascularization GOT, GPT, GLDH, AP, LDH, SDH, bilirubin, free fatty acid, and bile acid levels in serum increased progressively. Ammonia concentrations underwent a rapid increase in the first 9 h of coma development from 126.0 +/- 9.9 to 321.9 +/- 62.2 mumol/l. Most of the amino acids in serum were elevated and molar ratio of BCAA/AAA declined from 3.87 +/- 0.79 to 0.92 +/- 0.24. In the course of hemoperfusion ammonia was removed from the perfusate to 71% of the initial values using fresh and to 39% using preserved tissue. Correspondingly, there was an increase in urea concentrations. Amino acid metabolism was ameliorated during the perfusion; Fischer's quotient increased from 0.91 +/- 0.15 to 1.38 +/- 0.14 (fresh liver) and from 0.89 +/- 0.14 to 2.11 +/- 0.44 (preserved liver); neuroexcitatory amino acids Asp and Glu were markedly elevated. Energy charge of the liver cells increased and reached levels exceeding 0.5 in both experimental groups, a balanced energy metabolism was maintained and suggests active metabolization by the liver pieces. In comparison with fresh tissue, preserved liver cubes proved effective. We consider our artificial liver device capable of temporary hepatic support in acute necrosis of the liver and suppose that its efficiency can be potentiated by combining this system with other procedures.
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PMID:Successful treatment of hepatic coma by a new artificial liver device in the pig. 408 14

Previous reports have suggested the use of supraceliac aortic clamping in the surgical treatment of abdominal aortic aneurysm of difficult approach. The objective of the present report was to study the hepatic and renal metabolic changes of three groups of dogs submitted to temporary clamping (30 minutes) of the abdominal aorta at three different levels: below the renal arteries, infrarenal group (8 dogs); above the renal arteries, suprarenal group (9 dogs); above the celiac artery, supraceliac group (9 dogs). Blood bilirubin, alanine aminotransferase (ALT), aspartate aminotransferase (AST), urea nitrogen, and creatinine levels were measured before clamping and 5 minutes and 24 hours after reperfusion of the aorta. Bilirubin levels remained unchanged 5 minutes and 24 hours after reperfusion in all three groups. Alkaline phosphatase levels were significantly increased in all three groups 24 hours after reperfusion. ALT levels increased significantly in the supraceliac group and AST levels increased significantly in the infrarenal and supraceliac groups 24 hours after reperfusion of the aorta. However, despite these significant increases after reperfusion, the levels of these hepatic enzymes were still within the normal range for dogs. Urea nitrogen and creatinine levels showed that renal function did not change in any of the three groups. We conclude that supraceliac, infrarenal or suprarenal aortic clamping for 30 minutes do not promote any important changes in the hepatic or renal function of dogs.
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PMID:Supraceliac clamping in the surgical treatment of abdominal aortic aneurysm. An experimental study in dogs. 761 Mar 26

The incidence of acute cholecystitis complicating standard abdominal aortic aneurysm (AAA) repair has been reported between 0.3 and 18 per cent. This has prompted considerable debate regarding the management of cholelithiasis discovered incidentally during open aortic reconstruction. This study seeks to determine the incidence of cholelithiasis and acute cholecystitis after endovascular AAA repair and evaluate options for management. Between February 1996 and October 2001 492 patients underwent endovascular AAA repair. All the procedures were performed in the operating room under fluoroscopic guidance. Epidural (98.9%), local (0.5%), or general (1.7%) anesthesia was used during these cases. The incidence of cholelithiasis and acute cholecystitis was evaluated by CT scan and abdominal ultrasound. Serum measurements of alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, total and direct bilirubin, and amylase were performed and clinical assessment was conducted at 1, 6, and 12 months postoperatively and annually thereafter. The mean age of these patients was 76.6 years; 84% were male. Comorbid medical conditions were present in all patients (average 3.5 conditions/patient). Follow-up ranged from 2 to 35 months (mean 12.8 months). Endovascular stent graft deployment was successful in 486 of the 492 patients (98.8%). Six patients were converted to standard open repair because of inability to achieve successful endovascular aneurysm repair. The perioperative major morbidity rate was 14.9 per cent. Minor morbidity rate was 8.5 per cent. The perioperative mortality rate was 1.9 per cent. No deaths were related to biliary disease. Cholelithiasis was identified in 64 (13%) patients preoperatively. One of 64 patients with a prior Billroth II reconstruction for peptic ulcer disease developed jaundice 8 days after AAA repair as a result of choledocholithiasis that required surgical repair. One patient without gallstones developed acute acalculous cholecystitis on postoperative day 16 as determined on pathologic analysis of the gallbladder. A third patient who had gallstones identified on preoperative CT scan developed calculous cholecystitis 16 months after endovascular AAA repair. These two patients underwent uncomplicated laparoscopic cholecystectomy and recovered uneventfully. The incidence of postoperative symptomatic cholelithiasis is 1.6 per cent (one of 64). The incidence of postoperative acute cholecystitis was 0.2 per cent (one of 486) and was unrelated to the presence of gallstones. The incidence of delayed symptomatic cholelithiasis was 1.6 per cent (one of 64). Endovascular repair of AAA does not appear to predispose the patient to the development of symptomatic cholelithiasis during the perioperative period. Therefore a preoperative or intraoperative diagnosis of cholelithiasis does not necessitate cholecystectomy in the setting of planned endovascular AAA repair. Patients who develop cholecystitis after endovascular AAA repair may be effectively treated by standard laparoscopic techniques.
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PMID:Abdominal aortic aneurysmorrhaphy and cholelithiasis in the era of endovascular surgery. 1241 7