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目的:探讨瓦斯爆炸对真实巷道环境下大鼠急性冲击性肺损伤和呼吸功能指标时相变化的影响。方法:于2018年4月，用大型煤矿瓦斯爆炸试验巷道和爆炸测试系统模拟真实瓦斯爆炸巷道环境，固定笼具，设置爆炸参数。将72只SPF级SD大鼠按体重以完全随机分组法分为对照组、近距离组（160 m）和远距离组（240 m），各组内又分别设有创组（24 h组和48 h组，8只/组，6组共48只）和无创组（8只/组，3组共24只）。除对照组外，其余组大鼠在麻醉状态下置于不同距离点笼具内，将大鼠按照能使肺部受力的姿势摆放，实施瓦斯爆炸试验。无创组大鼠于爆炸后2、24、48、72和168 h用肺功能仪监测其呼吸功能指标的变化，7 d后麻醉处死；有创组大鼠分别于24、48和168 h后麻醉处死。对大鼠进行大体观察，肺组织湿/干重比值以及肺组织病理学检测。结果:与对照组比较，瓦斯爆炸2 h后近距离和远距离组大鼠呼吸频率（f）、每分钟通气量（MV）、最大吸气流速（PIF）、最大呼气流速（PEF）和潮气量达到50%时呼气流速（EF50）降低，呼吸间歇（PAU）、吸气时间（Ti）、呼气时间（Te）和放松时间（Tr）增加（n P<0.05）；48 h后远距离组大鼠潮气量（TV）、气道缩窄指数（Penh）、PAU、PIF均明显高于对照组，72 h后远距离组大鼠MV低于对照组（n P<0.05）；与对照组比较，168 h后近距离和远距离组大鼠Penh、PAU、Ti明显降低（n P<0.05）。不同距离组大鼠体重明显低于对照组（n P<0.05）。不同距离组大鼠肺组织大体及HE染色观察均显示，瓦斯爆炸引起肺水肿，肺毛细血管明显充血，大量炎性细胞、红细胞浸润。n 结论:真实巷道环境下瓦斯爆炸能够导致大鼠呼吸功能时相改变以及肺组织损伤，瓦斯爆炸致大鼠急性冲击性肺损伤模型初步建立成功，为进一步探索急性冲击性肺损伤致病机制奠定基础。“,”Objective:The aims of this study were to investigate the effect of gas explosion on rats and to explore the pulmonary function alterations associated with gas explosion-induced acute blast lung injury (ABLI) in real roadway environment.Methods:In April 2018, the large coal mine gas explosion test roadway and explosion test system were used to simulate the real gas explosion roadway environment, fixed the cage and set the explosion parameters. 72 SD rats, male, SPF grade, were randomly divided into nine groups by completely random grouping method according to their body weight: control group, close range group (160 m) , and long range group (240 m) . In each group, there were wound groups (24 h group and 48h group, 8/group, total 48 in six groups) and no wound groups (8/group, total 24 in three groups) . Except for the control group, the other groups were placed in cages at different distances under anesthesia, the experiment of gas explosion was carried out by placing the rats in a position that could force the lungs. The changes of respiratory function of the rats in the non-invasive group were monitored with pulmonary function instrument at 2 h, 24 h, 48 h, 72 h and 168h after the explosion, and were killed under anesthesia 7 days later; the rats in invasive groups were anesthetized and killed at 24 h, 48 h and 168 h, respectively. Gross observation, lung wet-dry ratio and lung histopathology were performed.Results:Compared with the control group, f (respiratory frequency, f) , MV (minute ventilation, MV) , PEF (peak expiratory flow rate, PEF) , PIF (peak inspiratory flow rate, PIF) and EF50 (1/2 tidal volume expiratory flow, EF50) of rats in the close and long range groups decreased significantly after gas explosion 2 h. PAU (respiration pause, PAU) , Te (expiratory time, Te) , Ti (inspiratory time, Ti) and Tr (relaxation time, Tr) were significantly increased (n P<0.05) . After 48 h, TV (tidal volume, TV) , Penh (enhanced respiration pause, Penh) , PAU, and PIF of rats in the long range group were significantly increased (n P<0.05) . After 72 h, MV in the long range group was significantly decreased (n P<0.05) . Compared with the control group, Penh, PAU, Ti and Te were significantly decreased after 168 h in the close and long range groups, with statistical significance (n P<0.05) . At the same time, the body weight of rats in different range groups was significantly decreased (n P<0.05) . In addition, both HE staining and routine observation of lung tissues of rats in different range groups showed that gas explosion caused pulmonary edema, obviously congested pulmonary capillaries, a large number of inflammatory cells and infiltrated red blood cells.n Conclusion:Gas explosion in real roadway environment can cause the change of respiratory function phase and lung tissue damage in rats, suggesting that the model of gas explosion-induced ABLI has been initially established successfully, which would provide a basis for further study on the pathogenesis of ABLI.