摘要
目的 探讨内皮素 (endothelin -1,ET -1)、一氧化氮 (NO)在血吸虫病门静脉高压性肺血管病变发病机制中的作用。方法 运用腹部敷贴法感染血吸虫尾蚴形成血吸虫病肝硬化门静脉高压症动物模型 ,模型组 (M组 ) 10只和正常对照组 (N组 ) 10只 ,应用免疫组织化学法对动物模型的肺组织中的ET -1、一氧化氮合酶 (nitricoxidesynthase ,NOS)进行定位性研究 ,并以正常兔作对照。结果 感染血吸虫尾蚴 12 0d后 ,肝硬化门静脉高压症动物模型成功 ,模型组肺组织中ET -1、NOS阳性细胞的表达均明显增多 ,染色增强 ,计算机图像定量分析示两组光灰度值和光密度值均具有显著性差异 (P <0 .0 1)。结论 ET -1、NOS在血吸虫病门静脉高压兔肺血管中的表达明显增强 ,表明ET -1、NO在血吸虫病门脉高压性肺血管病变发病机制中具有重要意义。
Objective To investigate the possible role of endothelin-1 (ET-1) and nitric oxide (NO) in the pathogenesis of portal hypertensive pulmonary vasculopathy in schistosomal cirrhosis.Methods The experimental group included 10 rabbits infected percutaneously with cercariae of schistosomiasis japonica.The control group included 10 normal rabbits.The distribution of ET-1 and NOS in the lung was studied by immunohistochemistry staining.The normal rabbits served as control group.Results 120 days after infection percutaneously with cercariae of schistosomiasis japonica,the rabbits in experimental group had pathologic changes.Both ET-1 and NOS-containing cells were more abundant in distribution and richer in color in the lung tissue of portal hypertension than those in the control group.There were significant differences between the two groups in the parameter of area,lightness and gray (P<0.01).Conclusion The expression of ET-1 and NOS in the lung vessels of portal hypertensive rabbits with schistosomal cirrhosis was obviously increased,suggesting that both ET-1 and NO might play an important role in the pathogenesis of portal hypertensive pulmonary vasculopathy.
出处
《临床外科杂志》
2005年第3期156-158,共3页
Journal of Clinical Surgery
基金
国家自然科学基金资助项目 (编号 :30 1 70 92 0 )
