Objective To evaluate the relationship between hypertriglyceridemia and acute pancreatitis.Methods Data was analyzed from 41 patients with acute pancreatits from Apr.1998 to Oct.2000 in our hospital.Of the 13 patients(GroupⅠ) with plasma TG level being higher than 11.3 mmol/L, 8 accompanied with gallstone(61.5%)and 5 without gallstone(38.5%)of the 28 patients (GroupⅡ) with plasma TG level being lower than 11.3 mmol/L,19 accompanied with gallstone(47.3%)and 9 without gallstone(52.7%)RANSON score,morbidity of complications and the level of ALT and AST were compared between two groaps.The correlation between TG and RANSON score was analysed.Results There were significant difference between the two groups on RANSON score,morbidity of complications and level of ALT and AST(P0.05).Conclusion There is an close relationship between hypertriglyceridemia and acute pancreatitis,the high level of plasma TG plags a key a role in acute pancreatitis,patients with acute pancreatitis with hypertriglyceridemia are more likely to have higher morbidity of complications and liver function aggravating.

Objective To investigate the effect of ischemia reperfusion (I/R) injury on apoptosis of pancreatic cells in rats with acute pancreatitis(AP). Methods Fifty four SD rats were randomized into 3 groups: pancreatitis group ( n =24), I/R injury group ( n =24) and control group ( n =6). The animal model of AP was induced by retrograde injection of 3% sodium taurocholate into biliopancreatic duct in rats. Pancreatic I/R was caused by blocking the inferior splenic artery and removing the clamp after AP induction. At 1 h, 3 h, 6 h and 12 h, groups of rats were sacrificed. A terminal deoxynucleotidyl transferase mediated dUTP biotion nick end labeling (TUNEL) was used to detect pancreatic apoptosis, and histological changes of the pancreas were observed. Results Pancreatic hemorrhage, necrosis were respectively observed in the pancreatitis rats at 6 h and the I/R injury rats at 1 h. Histological changes of the pancreatitis rats at 1 h and 3 h were only congestion and edema. Apoptoic acinar cells increased after AP induction, the peak respectively appeared at 6 h in the pancreatitis rats and at 3 h in the I/R injury rats. Compared with the pancreatitis rats, apoptosis index (AI) of the I/R injury rats was significantly higher at 1 h and 3 h ( P

Objective To investigate the effect of tuftsin and its inhibitor on pancreas microcirculation in acute pancreatitis(AP). Methods Sprague Dawley (SD) rats were randomly divided into five groups. Murine AP model was produced by retrograde injection of 4% sodium taurocholate into pancreatic duct, tuftsin or its inhibitor was injected at a dosage of 75 ?g/kg. At the time of 0,3, 6, 12 h, pancreas was harvested for pathology of microthrombus. esults Microthrombus in control group was not different with that in tuftsin group; At the time of 3、6 and 12 h microthrombus in other 3 groups significantly increased than control group and tuftsin group; With time, microthrombus in AP group、AP+ tuftsin group and AP+inhibitor group increased steadily and statistically significant; Tuftsin inhibitor significantly decreased microthrombus at the time of 6、12 h.Conclusions In acute pancreatitis tuftsin deteriorated pancreas microcirculation, which could be partially reversed by the administration of tuftsin inhibitor.