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

pancreatitis in rats

Background: Many interrelationships exist between the thyroid gland and the gastrointestinal tract. Several past and recent studies have shown that the thyroid gland profoundly influences the structure and function of the exocrine pancreas in the rat. In the present study we investigated the effect of methimazole (METZ), an antithyroid drug, on cerulein induced acute pancreatitis (AP) in rats.Methods: Rats were divided into 3 groups (10-12 weeks age, 200-250 g weight, n: 10). Group B was made hypothyroid with methimazole 5 mg/kg daily for 10 days and the others were untreated euthyroid groups. After 10 days, acute pancreatitis was induced with four doses of 20 mug/kg body weight of cerulein administered s.c at hourly intervals in group A and B while the control group C was given 4 doses of 1 ml saline. Pancreas wet weight (mg), plasma amylase activity (IU/l) and pancreatic histology were used as endpoints to quantify the severity of the AP.Results: Plasma tri-iodothyronine (T3) (ng/dl) and thyroxine (T4) (mug/dl) levels were significantly reduced after METZ treatment for 10 days (p < 0.01). METZ pretreatment reduced significantly the cerulein induced increase in pancreatic weight (1205 +/- 12 mg in METZ treated AP group versus 1617 +/- 14 mg in AP group, p < 0.05) and the rise in amylase activity (7078 +/- 816 IU/l in METZ treated AP group versus 8611 +/- 830 IU/l in AP group p < 0.05).Conclusion: METZ reduces the severity of cerulein induced AP in rats. This effect might be through its antithyroid property

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

WOS: A1994NH9090235