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目的初步探讨内源性NO在全氟异丁烯(perfluoroisobutylene,PFIB)急性吸入性肺损伤中的作用。方法雄性SD大鼠,随机分为对照和PFIB染毒后1,2,4,8,16和24 h活杀组,每组4只大鼠。其中PFIB染毒组行全身暴露动态吸入PFIB染毒(剂量为140 mg/m3×5 min),对照组行过滤空气暴露。分别在染毒前(对照组)与染毒后相应时间点,收集右肺组织、血清及左肺支气管肺泡灌洗液(bronchoalveolar lavage fluid,BALF)等标本,3H-精氨酸法测定肺组织内皮型一氧化氮合酶(eNOS)及诱导型一氧化氮合酶(iNOS)活力,酶法测定BALF及血清中NO(NO2-/NO3-)含量。结果肺组织eNOS活力在染毒后8 h内呈下降趋势,而iNOS与之相反,呈逐渐上升趋势,但与对照组比较,均没有显著差异;8 h后两者逐渐恢复至染毒前水平。血清及BALF中NO含量变化与iNOS活力相似。结论内源性NO及其合酶在PFIB急性吸入染毒前后变化不明显,在PFIB急性吸入性肺损伤中的作用尚不明确,其病理学意义有待进一步探讨。
Objective To investigate the role of endogenous nitric oxide (NO) in acute inhalation lung injury induced by perfluoroisobutylene (PFIB). Methods Male Sprague-Dawley rats were randomly divided into control and 1, 2, 4, 8, 16 and 24 h post-PFIB exposure groups, 4 rats in each group. The PFIB exposure group was exposed to PFIB (total dose 140 mg / m3 × 5 min). The control group was exposed to filtered air. Right lung tissue, serum and bronchoalveolar lavage fluid (BALF) in the left lung were collected before exposure (control group) and at the corresponding time points after exposure. The lung tissues were harvested by 3H-arginine assay Endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS) were measured by enzyme-linked immunosorbent assay (ELISA). The contents of NO (NO2- / NO3-) in BALF and serum were determined by enzyme-linked immunosorbent assay. Results The eNOS activity of lung tissue tended to decrease within 8 h after exposure, but iNOS was in the opposite trend, but no significant difference compared with the control group. After 8 h, the two returned to pre-exposure levels . Changes in NO content in serum and BALF were similar to iNOS activity. Conclusion The changes of endogenous NO and its synthase are not obvious before and after acute inhalation of PFIB. The role of endogenous NO and its synthase in PFIB acute lung injury remains unclear. The pathological significance remains to be further explored.