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目的 探讨一氧化氮合成酶 (INOS ,eNOS)在高氧所致急性肺损伤发病过程中的作用。方法 将 5 4只小鼠置于密闭的氧气室暴露于 >95 %的高氧 ,另 18只小鼠呼吸正常空气作为对照组 ;分别于 2 4、 4 8h和 72h取出小鼠 ,评价肺损伤程度同时进行支气管肺泡灌洗液细胞分类和计数 ;免疫组织化学测定肺组织iNOS和eNOS的表达及组织分布。结果 高氧能引起急性肺损伤伴支气管肺汽灌洗液细胞总数、巨噬细胞、中性粒细胞数均明显增加 ;免疫组织化学研究显示iNOS和eNOS蛋白主要表达于气道上皮细胞、血管平滑肌细胞和巨噬细胞的胞浆中 ,它们在气道上皮细胞的表达在高氧环境下明显升高。结论 在高氧环境下一氧化氮合成酶通过促进肺组织中一氧化氮合成从而在高氧所致的急性肺损伤过程中发挥重要作用。
Objective To investigate the role of nitric oxide synthase (INOS, eNOS) in the pathogenesis of acute lung injury induced by hyperoxia. Methods Fifty-four mice were exposed to> 95% hyperoxia in oxygen chamber and the other 18 mice were given normal air as control. Mice were sacrificed at 24, 48, and 72 hours respectively to evaluate lung injury At the same time, the bronchoalveolar lavage fluid cells were sorted and counted. The expression and distribution of iNOS and eNOS in lung tissue were detected by immunohistochemistry. Results Hyperoxia caused a significant increase of the number of total cells, macrophages and neutrophils in bronchoalveolar lavage fluid of acute lung injury. Immunohistochemistry showed that iNOS and eNOS protein were mainly expressed in airway epithelial cells, vascular smooth muscle In the cytoplasm of cells and macrophages, their expression in airway epithelial cells is significantly elevated under hyperoxia. Conclusion Nitric oxide synthase plays an important role in the process of hyperoxia-induced acute lung injury by promoting nitric oxide synthesis in lung tissue under hyperoxia.