Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0162871 (abdominal aortic aneurysm)
8,664 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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 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

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

The role of CD18 antibody (anti-CD18) in remote and local injury in a model of ruptured abdominal aortic aneurysm repair was investigated. Rats were divided into sham, shock, clamp, and shock + clamp groups. Shock + clamp animals received anti-CD18 or a control monoclonal antibody. One hour of hemorrhagic shock was followed by 45 min of supramesenteric aortic clamping. Intestinal and pulmonary permeability to (125)I-labeled albumin was determined. Myeloperoxidase (MPO) activity, F(2)-isoprostane levels, and transaminases were also measured. Only shock + clamp resulted in statistically significant increases in pulmonary and intestinal permeability, which were associated with significant increases in MPO activity and F(2)-isoprostane levels. Treatment with anti-CD18 significantly decreased intestinal and pulmonary permeability in shock + clamp animals. These reductions were associated with significantly reduced intestinal and hepatic MPO activity and pulmonary F(2)-isoprostane levels and reduced alanine and aspartate aminotransferase levels; however, anti-CD18 had no effect on intestinal or hepatic F(2)-isoprostane levels or on pulmonary MPO activity. These results suggest CD18-dependent and -independent mechanisms of local and remote organ injury in this model of ruptured abdominal aortic aneurysm.
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PMID:A CD18 monoclonal antibody reduces multiple organ injury in a model of ruptured abdominal aortic aneurysm. 1040 95

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