一氧化氮合酶蛋白和基因在肝肺综合征大鼠肺组织中的表达

Expression of Nitric Oxide Synthase Protein and Gene in Lung Tissue of Rats with Hepatopulmonary Syndrome

目的 探讨一氧化氮 (NO) 在肝肺综合征 (HPS) 发生机制中的作用。方法 采用 Wistar大鼠行胆总管结扎术 (CBDL) 制备HPS动物模型, 应用免疫组化方法观察内皮型一氧化氮合酶 (eNOS) 和诱导型一氧化氮合酶(iNOS) 蛋白在肺血管的表达和分布特点, 采用RT PCR方法检测肺组织中eNOS、iNOS mRNA的表达。结果 CB- DL组肺血管eNOS染色强度较假手术组显著升高 (P<0 .01), 而 iNOS表达在两组间差异无显著性意义 (P>0 .05);CBDL组大鼠肺组织eNOS mRNA的表达较对照组增高 (P<0. 01), 两组iNOS mRNA的相对表达量差异无统计学意义; 相关分析表明, 肺组织中eNOS mRNA水平与肺泡动脉氧分压差 (A- aDO2) 显著相关 (r=0. 920 1, P<0. 01)。结论 HPS时内皮细胞eNOS表达增强可能是肺血管NO增多的主要原因。

Objective To explore the role of nitric oxide (NO) in the pathogenesis of hepatopulmonary syndrome (HPS).Methods The HPS model of Wistar rats was established by common bile duct ligation (CBDL).The expression and localization of endothelium NOS (eNOS) and inducible NOS (iNOS) in pulmonary vessels were studied by immunohistochemical staining.By using RT-PCR,the expression levels of eNOS,iNOS mRNA in lung tissues were detected.Results There was a notable increase of eNOS staining in pulmonary endothelium of CBDL group as compared with control (P<0.01),while no remarkable change of iNOS staining was observed (P>0.05).The pulmonary eNOS mRNA expression in CBDL group was higher than in control group (P<0.01).However,the iNOS mRNA level between two groups had no significant difference.The level of eNOS mRNA was correlated with A-aDO 2 positively (r=0.920 1,P<0.01).Conclusion The enhanced expression of eNOS in endothelium may play the major role in the increased NO release of pulmonary vessels.