纳屈酮对大鼠急性出血坏死性胰腺炎致胰性脑组织损害的治疗作用

目的 探讨大鼠急性出血坏死性胰腺炎（AHNP）并发胰性脑组织损害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、胰性脑组织损害组（pancreatic encephalopathy,PE)及纳屈酮（NTX）治疗组，分别于6、12、24小时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、脑系数及胰腺和脑组织病理学改变。结果 与对照组比较，PE组6、12、24小时血浆及脑组织中MDA含量及PLA2活性升高，SOD活性下降；光镜下见PE组6、12及24小时胰腺红细胞渗出，、炎性细胞浸润及灶性坏死，脑组织水肿、点状出血和脱髓鞘改变；6小时电镜下见胰腺细胞线粒体肿胀，模糊，粗面内质网扩张；12小时线粒体破损，粗面内质网脱颗粒；24小时线粒体及粗面内质网破裂，次级溶酶体出现。NTX治疗组各时相血浆及脑组织MDA含量及PLA2活性较PE组低，SOD活性却较PE组高；且胰腺及脑组织的损害程度减轻。结论 大鼠AHNP模型可引发胰性脑组织损害；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；延长大鼠生存时间及降低其病死率。

THERAPEUTIC EFFECT OFNALTREXONE ON PANCREATIC ENCEPHALOPATHY INDUCED BY ACUTE HEMORRHAGIC NECROTIZINGPANCREATITIS IN RATS

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.