内源性一氧化氮在急性出血坏死性胰腺炎发病中的作用  

Role of Endogenetic NO in the Pathogenesis of Acute Hemorrhagic and Necrotic Pancreatitis

作　　者：赵敏[1] 陈瑞芬[1] 周以键[1] 王兴翠[2] 

机构地区：[1]首都医科大学病理解剖学教研室 [2]首都医科大学中心实验室

出　　处：《首都医科大学学报》2003年第3期243-246,共4页Journal of Capital Medical University

摘　　要：为探讨内源性一氧化氮 (NO)在急性出血坏死性胰腺炎 (AHNP)发病中的作用 ,胰胆管内逆行注射 5 %牛磺胆酸钠 ,建立大鼠急性出血坏死性胰腺炎模型 ,通过光镜观察胰腺的病理变化 ,用免疫组化SP法测定胰腺微血管内皮细胞内eNOS的表达 ,用Westernblot分析胰腺组织内iNOS的表达。结果 :诱导AHNP后 5min就出现胰腺微血管的病变 ,并伴有腺泡细胞凝固性坏死。随着时间的延长 ,上述病变加重。术后 1 0min ,胰腺间质小血管内皮细胞表达eNOS开始显著增高 (P <0 .0 5 ) ,并随着疾病的发展而逐渐增高。术后 5min,胰腺组织内iNOS表达开始增高 (P <0 .0 5 ) 。To investigate the role of endogenetic NO in the pathogenesis of acute hemorrhagic and necrotic pancreatitis, AHNP was induced in rats (300～350 g) by intraductal administration of 5% sodium taurocholate. The pathologic morphologic changes of pancreatic blood micro-vessel and acinus were observed under light microscope. The expression of eNOS in endothelium was examined through Immunohistochemistry and the Western blot analyses were performed on the expression of iNOS in tissue. The injuries were found in pancreatic micro-vessel 5 min after the inducement, accompanied by acinus coagulation necrosis. These changes were aggravated with the development of the disease. The expression of eNOS in endothelium of pancreatic micro-vessel began to increase significantly 10 min after the administration (P<0.05) and continue to increase with the development of the disease. The significant increase of the expression of iNOS in pancreatic tissue began at 5 min after the administration (P<0.05) and continued to 6 h after the inducement.

关 键 词：内源性 N0 急性出血坏死性胰腺炎 AHNP 一氧化氮合成酶 

分 类 号：R657.51[医药卫生—外科学]