Biliary sphincterotomy plus dilation with a large balloon for bile duct stones that are difficult to extract

WOS: 000180730000002PubMed ID: 12556775Background: Bile duct stones are still present in 10% to 15% of patients after the application of conventional endoscopic extraction techniques and require additional procedures for duct clearance. In the vast majority of these cases, there are 2 main problems: large stone size (>15 mm) and tapering of distal bile duct. Methods: Fifty-eight patients in whom endoscopic sphincterotomy and standard basket/balloon extraction were unsuccessful in the removal of bile duct stones underwent dilation with a 10- to 20-mm diameter (esophageal/pyloric type) balloon at the same session. In 18 patients with tapered distal bile ducts (Group 1), 12- to 18-mm diameter balloon catheters were used to enlarge the orifice. In 40 patients with square, barrel shaped and/or large (>15mm) stones (Group 2), the sphincterotomy orifice was enlarged with 15- to 20-mm diameter balloon catheters. After dilatation, standard basket/balloon extraction techniques were used to remove the stone(s). Results: Stone clearance was successful in 16 patients (89%) in Group 1 and 35 (95%) in Group 2. Complications occurred in 9 (15.5%) patients. Conclusion: Dilation with a large-diameter balloon after endoscopic sphincterotomy is a useful alternative technique in patients with bile duct stones that are difficult to remove with standard methods

Ketotifen ameliorates development of fibrosis in alkali burns of the esophagus

WOS: 000223007900008PubMed ID: 15108014An experimental study was performed to investigate the efficacy of ketotifen, which is a mast cell stabilizer and histamine H-1-receptor antagonist, on the prevention of stricture development after esophageal caustic injuries in the rat. Caustic esophageal burn was created by applying 37.5% NaOH to the distal esophagus. Forty rats were divided into four equal groups. Group A (sham) animals were uninjured. Group B rats were injured but untreated. Group C rats were injured and received ketotifen (1 mg/kg/day) via the oral route. Group D rats were injured and received ketotifen (1 mg/kg/day) via the intraperitoneal route. Efficacy of the treatment was assessed on day 28 by measuring the stenosis index and histopathologic damage score and biochemically by determining tissue hydroxyproline content. The stenosis index in group B (0.93+/-0.22) was significantly increased compared with group A (0.39+/-0.06, p <0.05), group C (0.42+/-0.09, p <0.05), and group D (0.35+/-0.07, p <0.05). The hydroxyproline level (mug/mg wet tissue) was significantly increased in group B (1.31+/-0.08, p <0.05) compared with group A (0.69+/-0.16, p <0.05), group C (1.06+/-0.16, p <0.05), and group D (0.95+/-0.12, p <0.05). In group B the histopathologic damage score was significantly higher than in groups C (p <0.05) and D (p <0.05). There was no significant difference between group C and group D in terms of all parameters evaluated. Treatment with ketotifen decreased tissue hydroxyproline levels, histological damage, and the stenosis index. We conclude that ketotifen has a preventive effect in the development of fibrosis in an experimental model of corrosive esophagitis in rats

Possible role of glutathione in prevention of acetaminophen-induced hepatotoxicity enhanced by fish oil in male Wistar rats

WOS: 000072469800004PubMed ID: 9482353It has been reported that fish oil protects the rat liver against acetaminophen (APAP) induced toxicity; however, this finding is controversial. The present study was undertaken to investigate the effects of fish oil-enriched diet on APAP-induced liver injury in Wistar rats. Rats were fed a diet supplemented with either 8% fish oil or 8% corn oil, or standard rat feed for 6 wk. After an overnight fast, rats in each group were given either 2 g/kg APAP or saline orally. Our findings showed that APAP increased serum alanine aminotransferase (ALT) and that this rise was potentiated in the presence of dietary fat. Further fish oil ingestion increased the glutathione (GSH) content in rat liver; however, this was not effective in protecting liver from APAP-induced toxicity. Data suggest that GSH may be necessary to detoxify APAP metabolites, which are known to induce hepatotoxicity but are increased by dietary fat

The Influence of Laparoscopy on Lower Esophageal Sphincter Pressure - Does Increased Intraabdominal Pressure Lead To Gastroesophageal Reflux

WOS: A1994NH9090235

Cytoprotective Effect of Allopurinol on Gastric-Mucosa In Rats

WOS: A1992JP3450023

pancreatitis in rats

Aim. In this study we aimed to clarify the role of mast cells in the development and progression of inflammation in cerulein-induced acute pancreatitis (AP) in rats. We have also examined the effects of ketotifen;, a mast-cell stabilizing agent in the treatment of acute pancreatitis and its relation with nitric oxide (NO) synthesis.Methods. In the first part of the study we planned to examine the effects mast cell stabilization in acute pancreatitis, while the second part was focused on examining the relation between NO synthesis and the potential effects of ketotifen in AP. Wistar albino rats were randomly divided into 6 groups (In: 10). In the first part of the study, AP was induced by four subcutaneous (sc) injections of 20 mug/kg body weight of cerulein at hourly intervals in Groups A and B while Group C was treated with saline as the control group. Group B was pretreated with ketotifen 1 mg/kg (ip). In the second part, the study design was similar except for the inhibition of nitric oxide synthesis by N-nitro L-arginine methyl ester (L-NAME) 30 mg/kg (ip) in Groups D, E and F. Group D was treated with L-NAME and cerulein and Group E was treated with ketotifen, L-NAME and cerulein. Group F was treated with L-NAME and saline as the control group. Serum amylase activity and pancreatic myeloperoxidase activity (MPO) were measured. Pancreatic histology and mast-cell count in pancreatic tissue were evaluated.Results. Mast cell count was found to be increased in the pancreatic tissue in cerulein-induced AP. (2.93 +/- 0.26 vs 1.98 +/- 0.26; p<0.001). Ketotifen treatment significantly reduced cerulein induced edema (1.30 +/- 0.21 vs 0.70 +/- 0.15; p<0.001), neutrophil infiltration (1.50 +/- 0.16 vs 0.60 +/- 0.16 p<0.001) and attenuated the increase in amylase (4394.0 +/- 149.5 U/L vs 3350.5 +/- 216.9 U/L; p<0.05) and MPO activity 1.14 +/- 0.13 U/gr tissue vs 0.54 +/- 0.08 U/gr tissue; p<0.001). Mast-cell count in pancreatic tissue was also decreased significantly with ketotifen pretreatment (2.93 +/- 0.26 vs 1.70 +/- 0.21; p<0.05). Inhibition of NO synthesis with L-NAME treatment decreased the beneficial effects of ketotifen.Conclusion. It seems likely that mast cell activity may play an important role in the initiation and progression of acute pancreatitis. Ketotifen treatment may reduce the severity of AP in rats. The protective action of ketotifen in cerulein-induced acute pancreatitis is most probably owing to mast cell stabilization and stimulation of NO synthesis

Effects of pentoxifylline on gastric acid secretion in rats

Abstract Not Availabl