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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 role of endothelin-1 (ET-1) and nitric oxide (NO) in the pathogenesis of portal hypertension pulmonary hypertension in schistosomiasis. Methods The animal model of Schistosoma japonicum cirrhosis and portal hypertension was infected with cercariae of Schistosoma japonicum by abdominal application method. Ten rabbits in model group (M group) and 10 normal rabbits (N group) were used as control. Immunohistochemistry (ET-1) and nitric oxide synthase (NOS). The normal rabbits were used as controls. Results The cercariae of Schistosoma japonicum infected with cercariae 120 days later, the model of liver cirrhosis and portal hypertension were successfully established. The expression of ET-1 and NOS positive cells in the model group were significantly increased and the staining was enhanced. The quantitative analysis of computer image showed that the light gray value and light Density values were significantly different (P <0. 01). Conclusions The expression of ET-1 and NOS in pulmonary blood vessels of rabbits with schistosomiasis is significantly increased, indicating that ET-1 and NO are important in the pathogenesis of portal hypertension-induced pulmonary vascular disease.