TO investigate the relationship between endotoxemia and structural change in the pancreatic tissue and therapeutic effects of naltrexone (NTX) on experimental acute hemorrhagic necrotizing pancreatitis in rats. The model of acute hemorrhagic necrotizing pancreatitis (AHNP) of rats was induced by retrograde injection of 5% sodium taurocholate into the pancreatic duct. One hundred and ten Wistar rats were randomly divided into three groups: control group (n=20),AHNP group (n=45) and NTX treatment (n=45) group. The weight of pancreas and plasma levels of amylase and endotoxin were measured as well as changes of the pancreatic histology were examined by light and electric microscope in 6h, 12h, 24h after operation. Results as compared with control groups , amylase and endotoxin in AHNP group were significantly higher in the plasma and the damage to pancreatic tissue was increased in severity as observed with light and electric microscopes in 6h, 12h, 24h after operation. Comparison between NTX treatment groups with AHNP groups demonstrated that amylase and endotoxin were significantly decreased in the plasma, and the damage to pancreatic tissue was reduced in NTX treatment phase. Conclusion these results showed that endotoxemia was induced by AHNP, but NTX decreased the edotoxin level in the plasma and improved the damage of pancreatic tissue. The lethality was significantly lowered and average survival time was prolonged during NTX treatment of AHNP.
Objective To study the relationship between oxygen free radical and phospholipase A2 and therapeutic effect of naltrexone (NTX) on experimental pancreatic encephalopathy (PE) induced by acute hemorrhagic necrotizing pancreatitis (AHNP) in rats. Methods A model of experimental PE in AHNP was induced by retrograde injection of 5% sodium taurocholate into the pancreatic duct. The rats were randomly divided into three groups: control group, PE group and NTX group. The plasma and cerebral levels of malondialdenhyde(MDA), scavengers superoxided ismutase(SOD), and phospholipase A2 (PLA2) were determined in both PE and NTX groups. Changes of the pancreatic and cerebral histology were examined by light and electric microscopy. Results In NTX treatment phase, the MDA and PLA2 were significantly fall, while SOD was increased in the plasma and cerebral tissue, the damage to pancreatic and cerebral tissue was emiliorated. Conclusion The experimental model of PE on rats is an ideal one for PE investigation. NTX could decrease oxygen free radicals and PLA2 activity and improve the damage to cerebral and pancreatic tissue. The lethality rate in rats of PE is significantly low after NTX treatment.
