老年大鼠肾缺血再灌注后肺损伤一氧化氮合酶的变化与意义

Expression NOS in lung injury following renal ischemia reperfusion and ite significance in aged rats

目的:研究大鼠肾缺血/再灌注后急性肺损伤时,内皮型一氧化氮合酶(eNOS)和诱导型一氧化氮合酶(iNOS)的表达及其在急性肺损伤发生中的作用。方法:采用夹闭双侧肾动、静脉45min后恢复血流的方法制作RIRI模型,免疫组织化学方法检测肺组织中iNOS和eNOS的表达,同时检测肺组织中MDA、MPO、W/D和NO2-/NO3-值,肺组织形态学观察以评价肺损伤的程度。结果:与control组比较,I/R组eNOS表达增强,iNOS表达减弱,MDA、MPO、W/D和NO2-/NO3-值增加,肺组织充血、炎细胞浸润,肺泡腔渗液;与I/R组比较,L-Arg组eNOS表达增强,iNOS表达减弱,NO2-/NO3-增加,MDA、MPO、W/D降低,肺组织损伤有减轻趋势,AG组eNOS表达无明显变化,iNOS活性降低,NO2-/NO3-减少,MDA、MPO、W/D降低,肺组织损伤有减轻趋势。结论:肾缺血/再灌注急性肺损伤过程中,eNOS表达增加,NO生成增多,在肺损伤发生中有一定的保护作用。

Objective：To investigate the expression and role of inducible NOS（iNOS） and endothelial NOS（eNOS） in acute lung injury following renal ischemia reperfusion（45min/24h） in rats.Methods： The model of RIRI was induced by bilateral clamping the renal artery and vein for 45 min followed by reperfusion. The expression of iNOS and eNOS was examined with immunohistological staining. The lung tissue of each group was subjected to assay of content of MDA, MPO,W/D and NO2-/NO3-. The pulmonary morphologic changes were observed under microscope respectively.Results： Compared with control group, the expression of eNOS upregulate and the expression of iNOS downregulate in I/R group.The parameters of MDA, MPO, W/D and NO2-/NO3-in pulmonary tissue were significantly increased in I/R groups,Compared with those of the control group. Based on the results of pulmonary pathology, the congestion and infiltration of inflammatory cells existed obviously in IR group. Compared with IR group , the expression of eNOS upregulate and the expression of iNOS downregulate,the contents of NO2-/NO3-increase and MDA,MPO,W/D decreases ,plumonary tissue injury lighten in L-Arg group. There was no statistical difference of eNOS between I/R group and AG group. compared with IR group ,the expression of iNOS downregulate, the value of MDA,MPO,W/D decreased and plumonary tissue injury lighten in AG group.Conclusion： The upregulated expression of eNOS and the increasing of NO possibly play a compensitivly protective role in acute lung injury following renal ischemia/reperfusion.