模拟失重大鼠肺组织显微结构和一氧化氮合酶表达的动态变化

Dynamic changes of microscopical structure and NOS expression in rat lung tissues under simulated weightlessness

目的 观察模拟失重对大鼠肺组织显微结构及其一氧化氮合酶(NOS)表达的影响,为模拟失重时肺组织的适应机制研究积累资料.方法 采用Wistar雄性大鼠-30°尾部悬吊模拟失重生理效应.常规光镜和免疫组织化学方法 观察悬吊7 d组(TS7)、14 d组(TS14)及对照组(Con)肺组织显微结构和结构型NOS(cNOS)、诱导型NOS(iNOS)表达.结果 TS7组大鼠出现肺实变、肺水肿、支气管黏膜内淋巴细胞浸润、肺泡内有红细胞及肺泡融合.TS14组大鼠肺病变较TS7组大鼠明显加重,表现为肺泡融合增多、肺泡内更多红细胞和肺泡壁增厚.各组大鼠肺组织cNOS表达区域主要为支气管上皮细胞、血管内皮细胞和平滑肌细胞,各组间表达水平无统计学差异.iNOS表达在TS7、TS14组血管内皮细胞和平滑肌细胞表达显著增多,其中TS14组血管内皮细胞表达量高于TS7组.结论 模拟失重大鼠肺组织形态学变化可能与肺循环iNOS表达增加有关.

Objective To observe dynamic changes of microscopical structure and nitric oxide synthase(NOS) expression in rat lung tissues under simulated weightlessness,and to collect the data for studies of the adaptive mechanism of local regulation in lung tissues. Methods Wistar male rats were -30° tail suspended to simulate the physiological effects of weightlessness. The microscopical structure,constitutive NOS(cNOS)and inducible NOS(iNOS)expression of rat lung tissues in control group(Con),7-day tail suspension group(TS7) and 14-day tail suspension group(TS14) were respectively observed with routine microscope and immunohistochemistry. Results The solid edema of lungs appeared in TS7 rats,accompanied with lymphocyte soakage in bronchial mucous membranes,red blood cells in alveolus and alveolar amalgamation. The pathological change was more obvious in the TS14 group than that in TS7 group,accompanied with more alveolar amalgamation,more red blood cells in alveolus and thicker alveolar walls. The cNOS expression regions of lung tissues in three groups were mostly the bronchial epithelium,vascular endothelial cells and vascular smooth muscle cells,but there were no significant differences among all groups. The iNOS expression of the TS7 and TS14 rat lung tissues increased significantly as compared with Con rats,which was more obvious in vascular endothelial cells of TS14 than TS7.Conclusion The morphological changes in lung tissues induced by simulated weightlessness are mainly due to the up-regulation of iNOS expression in pulmonary circulation.