血吸虫病门静脉高压兔食管下端血管病变的研究

目的:探讨血吸虫性门静脉高压兔食管下端的血管病变。方法:以腹部敷贴法感染血吸虫尾蚴的家兔为血吸虫性门静脉高压症的动物模型。采用HE染色、Masson三色染色、透射电镜观察食管下端黏膜下血管的病理变化。应用免疫组化和半定量Western免疫印迹方法检测ET1、cNOS、iNOS在食管下端的表达。结果:感染尾蚴120d后,食管下端黏膜下血管已有明显病理变化,与正常对照组相比ET1、cNOS、iNOS的表达明显增加(P<0.01),主要表达于食管黏膜毛细血管、黏膜下血管壁的内皮细胞。结论:门静脉高压症时,血管病变的产生可能既是血管对高动力循环状态的适应与代偿的结果,也是静脉曲张进一步发展和破裂出血的原因之一。ET1、cNOS、iNOS的高表达可能参与了血管病变的形成。

Experimental study on lower esophageal vasculopathy in rabbits with portal hypertension caused by schistosomal cirrhosis

Objective To study lower esophageal vasculopathy in rabbits with portal hypertension caused by schistosomal cirrhosis. Methods The experimental group included 10 rabbits infected percutaneously with cercariae of schistosomiasis japonica. The controls included 10 normal rabbits. HE stain, Masson trichrome stain and transmission electron microscope examination were used to observe pathologic pattern of the submucosal blood vessels in lower esophagus. Immunohistochemistry and quantitative analysis of Western blot were applied to detect the protein expression of ET,1, cNOS, iNOS. Results The experimental group rabbits presented pathologic changes in submucosa blood vessels. The expression of ET,1, cNOS, iNOS was significantly stronger in lower esophageal tissues of the infected rabbits than that of the controls(P<0.01), and their expression mainly occurred in capillaries of the esophageal mucosa and endothelial cells of the submucosal blood vessels. Conclusions In portal hypertension, vasculopathy is not only a mechanism of compensation to the high hemodynamic state, but also a result of progression of the lower esophageal varices.