门、腔静脉阻断与开放对门静脉高压模型犬肺组织与肺动脉iNOS、eNOS和ET表达的影响

Effect of portal-cavity clamped and opened on expression of iNOS、eNOS and ET in portal hypertension canine

目的观察门静脉和下腔静脉阻断与开放后门静脉高压模型犬肺组织和肺动脉的病理学特点及诱生型一氧化氮合酶(iNOS)、内皮型一氧化氮合酶(eNOS)和内皮素(ET)基因与蛋白表达的变化。方法正常家犬18只,随机均分为阴性对照组、对照组和门静脉高压模型组,进行门静脉和肝后下腔静脉阻断㈦开放实验。在术毕观察右下肺动脉和肺组织病理形态学特征,并检测肺组织和肺动脉iNOS、eNOS和ET基因与蛋白表达的变化。结果模型组与对照组肺组织和肺动脉在经历门、腔静脉阻断㈦开放后均存在不同程度病理形态学改变,但以模型组改变更为显著;模型组肺组织iNOS和肺动脉iNOS、eNOS基因和蛋白的表达显著强于阴性对照组和对照组(P<0.05)。结论肺组织和肺动脉在经历门、腔静脉阻断㈦开放后均存在明显的病理形态学改变。肺动脉iNOS和eNOS基因和蛋白表达水平明显上调,可能在一定程度上参㈦门静脉高压肝Σ植围术期肺循环的变化;而门静脉高压肝Σ植围术期易并发急性肺损伤则可能㈦肺组织中iNOS基因和蛋白表达水平上调有关。

Objective To observe changes of the pathological characteristic of lung and pulmonary artery after portal-cavity clamped and opened in portal hypertension canine, and investigate expression regularity of inducible nitric oxide synthase（iNOS）, endothelial nitric oxide synthase（eNOS） and endothelin（ET） in tissues of lung and pulmonary artery. Methods Eighteen canines were randomly divided into groups Ⅰ （negative control group）, Ⅱ （control group） and Ⅲ （model group）. Samples of lung and pulmonary artery were collected postoperatively. The pathological characteristic of lung and pulmonary arteries were analyzed. The mRNA and protein expression of iNOS, eNOS and. ET in tissues of lung and pulmonary artery were assessed. Results There were pathomorphological changes of pulmonary tissue and pulmonary artery after portal-cavity clamped and opened in group Ⅱ and Ⅲ. But they was more significant in group Ⅲ than those in the other groups. Compared with group Ⅰ and Ⅱ, the gene and protein expression of iNOS in lung increased significantly in group Ⅲ, the expression of iNOS and eNOS in pulmonary artery were also increased in group Ⅲ（P〈0.05）. Conclusions There are visible pathomorphological changes of pulmonary tissue and artery after portal-cavity clamped and opened. The expression ofiNOS and eNOS in pulmonary artery are increased, which may explain the perioperative changes of pulmonary circulation in portal hypertension canine. And the liability to acute lung injury may also be partly influenced by the expression of iNOS in lung.