大鼠吸入全氟异丁烯中毒后不同时间对内源性NO及其合酶活力的影响

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。

The time-course effect of perfluoroisobutylene inhalation on endogenous nitric oxide and its synthases activity in rats

Objective To investigate preliminarily the role of nitric oxide（NO） in perfluoroisobutylene（PFIB）-induced acute lung injury（ALI）.Methods Male SD rats were randomly divided into one control group and six PFIB-exposed groups which were executed at 1 h,2 h,4 h,8 h,16 h and 24 h after PFIB exposure,respectively,with 4 rats in each group.The PFIB-exposed groups were exposed to PFIB at the concentration of 140 mg/m3 for 5 min in a flow-past whole-body chamber while the control group was exposed to the filtered air in a similar manner.After execution at the corresponding time-point,the right lung,serum and brochoalveolar lavage fluid（BALF） from the left lung were collected and the nitric oxide synthase activity（both the endothelial and the inducible types,namely eNOS and iNOS）,the content of NO in the serum and BALF were measured.Results During the first 8 hours after PFIB exposure,the activity of eNOS in the lung tissue showed a trend of gradual declination but with no statistical significance detected when compared with the control group.The activity of iNOS in the lung tissue demonstrated an opposite tendency.Eight hours after PFIB exposure both types of NOSs began to gradually return to their baselines.The content of NO in the serum and BALF showed similar change profiles to those of iNOS activity.Conclusion No dramatic changes in the content of NO or in the activity of NOSs were found,suggesting the pathological significance of the endogenous NO system in the PFIB-induced ALI needs to be further clarified.