摘要
目的 :探讨大鼠急性出血坏死性胰腺炎 (AHNP)并发胰性脑病的机理及评价纳屈酮治疗效果。方法 :应用 5 %牛磺胆酸钠逆行胰胆管注射诱发大鼠AHNP并发脑组织损害模型。实验分为对照组、胰性脑病 (PE)组及纳屈酮 (NTX)治疗组 :分别于 6、12、2 4h检测血浆及脑组织脂质过氧化产物丙二醛 (MDA)含量、磷脂酶A2(PLA2 )活性、氧自由基清除剂超氧化物歧化酶 (SOD)活性、脑指数及胰腺和脑组织病理学改变。结果 :PE组 6、12、2 4h血浆及脑组织较对照组 :MDA含量、PLA2 活性升高 ;SOD活性下降。PE组光镜下 6、12、2 4h分别出现胰腺红细胞渗出、炎性细胞浸润、灶性坏死及脑组织水肿、点状出血、脱髓鞘改变。电镜下 6h胰腺细胞线粒体肿胀 ,嵴模糊 ,粗面内质网扩张 ;12h线粒体破损 ,粗面内质网脱颗粒 ;2 4h线粒体及粗面内质网破裂 ,次级溶媒体出现及泡心细胞绒毛断失。NTX治疗组较PE组 ;血浆及脑组织MDA含量、PLA2 活性下降及SOD活性升高 ;而且胰腺及脑组织损害减轻。结论 :大鼠AHNP模型可引发胰性脑病 ;NTX可降低血浆及脑组织氧自由基 (OFR)含量、PLA2 活性 ,同时增加SOD活性 ,进而减轻脑组织损害作用 ;从而 。
Objective:To study the relationship between oxygen free radical and phospholipase A 2 and therapeutic effect of naltrexone on experimental pancreatic encephalopathy induced by AHNP in rats.Methods:A model of experimental pancreatic encephalopathy(PE) emerged from acute hemorrhagic necrotizing pancreatitis(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. We studied the effects of morphine receptor blocker, naltrexone(NTX) during the rats of PE and measured the plasma and cerebral levels of malondialdehyde(MDA), scavengers superoxide dismutase(SOD), phospholipase A 2 and calculated the death rate as well as average survival time in rats of both PE and NTX groups. Changes of the pancreatic and cerebral histology were examined by light and electron microscopy. Results:In NTX treatment phase, the results demonstrated that MDA and PLA 2 were significant fall, besides SOD was increased in the plasma and cerebral tissue and the damage of pancreatic and cerebral tissue was reduced. Conclusion:The experimental modele of PE on rats is ideal to investigation of PE. NTX decreased oxygen free radicals, PAL 2 and improved the damage of cerebral and pancreatic tissue. The fatality rate in rats of PE was significantly lower in NTX treatment.
出处
《内蒙古医学院学报》
2000年第2期84-87,共4页
Acta Academiae Medicinae Neimongol
关键词
胰腺炎
脑病
自由基
磷脂酶A2
治疗
pancreatitis
encephalopathy
phospholipase A 2
free radical