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.
To study the role of endotoxin in acute hemorrhagic necrotizing pancreatitis (AHNP), the change of endotoxin were studied in rats AHNP models by injection of 5% sodium taurocholate 1 ml/kg into pancreatic duct, and the effects of recombinant interleukin-2 (IL-2) in the treatment of AHNP were observed in this experiment. The results indicated that endotoxin involved the aggravation of AHNP and was associated with the increase of serum phospholipas-2 (PLA2), and these mediators were positively correlated with severe degrees of pancreatic damage. The results also suggeste that IL-2 might inhibit the overexpression of endotoxin and PLA2 and mitigate the pancreatic injury and decrease the 72h-mortality rate of AHNP from 66.7% to 26.7% (Ｐ＜0.01). Endotoxin might play a major role in the pathogenesis of AHNP and IL-2 might have a potential role in the treatment of AHNP.
To evaluate the feasibility, safety and effectiveness of enteral nutrition (EN) via jejunostomy in the early postoperative period in patients with acute hemorrhagic necrotizing pancreatitis (AHNP), 38 patients were divided into the early group (start EN 3 or 4 days after operation) and the later group (start EN 7 days after operation). All patients received parenteral nutrition at first, then were transited to EN. The enteral nutrition liquid was transfused by continuous drip via jejunostomy in both groups. Levels of serum amylase, blood glucose, as well as the liver function were used as indices of tolerance. Symptoms and physical signs of abdominal pain as well as the level of serum albumin were used as the indices of effectieness. Patients tolerated the therapy well in both groups. Moreover, they enjoyed an earlier correction of hypoalbuminemia with more quickly improved serum albumin and no abdominal pain. Starting enteral nutrition in the early postoperative period is feasible, safe and efficacious for acute hemorrhagic necrotizing pancreatitis patients. It plays an important role in treating AHNP and improving curing rate.
To investigate changes of serum nitric oxide (NO) levels and therapeutic effects of sodium nitroprusside (SNP) in acute hemorrhagic necrotizing pancreatitis (AHNP) in rats, one hundred and twenty Wistar rats were divided into three groups randomly (forty in each group) animal models of AHNP group were produced by retrograde injection of 5% sodium taurocholate into pancreatobiliary duct.In the treatment group SNP (0.05mg/100g) was injected intraperitoneally after AHNP models established and then repeated three hours later. In the control group only retrograde injection of normal saline (0.5ml) into pancreatobiliary duct was performed. The results showed: compared with the treatment group, serum NO and SOD levels were significantly lower in AHNP group (Ｐ＜0.05); serum amylase levels and pancreatic indexes were markedly higher in AHNP (Ｐ＜0.01 and Ｐ＜0.05 respectively);the mortality in 24 hours was significantly higher and survival time was significantly shorter in AHNP group (Ｐ＜0.01).Pathologic changes of pancreas were significantly severe in AHNP group. From the above results we can draw the conclusion that NO plays an important role in the pathogenesis of AHNP and SNP has therapeutic effects on AHNP in rats.
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.
The model of acute hemorrhagic necrotizing pancreatitis (AHNP) was produced by retrograde forced injection of autogenous bile into the main pancreatic duct. The result showed that urgent surgical (transduodenal) intra-pancreatic duct drainage reduced the mortality rate of the experimental animals. Keeping the drainage patent and clear can both abate the pathological changes and promote the renovation of the dogs pancreas. So it can guide the clinical treatment in some way.