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目的观察密闭舱室内非金属材料燃烧释放有毒气体对大鼠肺毛细血管通透性及肺表面活性物质相关蛋白A的影响。方法建立密闭舱内动物烟雾吸入模型,将36只SD大鼠完全随机分为对照组及烟雾吸入后1、6、24、72h和7d组,观察吸入损伤后不同时相点肺组织的病理改变,肺水含量及肺通透指数的变化,采用RT-PCR法检测大鼠肺组织SP-AmRNA的表达。结果烟雾吸入后大鼠肺组织病理改变与急性肺损伤样的病理改变特征相似,24h为肺组织病理改变最严重期,在此期间动物的肺水含量也较对照组有明显增加(P<0.05);肺泡灌洗液及血清中蛋白含量在烟雾吸入后不同时相点均增高,肺通透性指数在1、6h和24h显著高于对照组(P<0.05);烟雾吸入后各时相点动物肺组织SP-AmRNA表达均降低,其中1、6、24h和72h组与对照组比较差异显著(P<0.01)。结论密闭舱室内非金属材料燃烧释放的毒性气体可引起肺泡毛细血管通透性的改变及肺表面活性物质相关蛋白A的降低,肺血管及间质之间液体交换障碍,导致肺水肿进而引发急性肺损伤。
Objective To observe the effects of toxic gases released by combustion of nonmetal materials in aseptic chambers on pulmonary capillary permeability and pulmonary surfactant-associated protein A in rats. Methods Airtight aerosol inhalation model was established. Thirty-six Sprague-Dawley rats were randomly divided into control group and 1, 6, 24, 72h and 7d groups after smoke inhalation. The pathological changes of lung tissue were observed at different time points after inhalation injury , Lung water content and pulmonary permeability index. The expression of SP-AmRNA in lung tissue of rats was detected by RT-PCR. Results After the inhalation of smoke, the pathological changes of lung tissue in rats were similar to those of acute lung injury. The pathological changes of lung tissue were similar at 24 h, and the lung water content of the rats was also significantly increased (P <0.05 ); Alveolar lavage fluid and serum protein levels increased at different time points after inhalation of smoke, pulmonary permeability index was significantly higher at 1,6h and 24h (P <0.05); smoking after each phase The expression of SP-AmRNA in the lung tissue of the point animals was decreased, and the difference was significant (P <0.01) between the 1, 6, 24 h and 72 h groups and the control group. Conclusions Toxic gases released by the combustion of nonmetallic materials in airtight compartments may cause alveolar capillary permeability changes and decrease of pulmonary surfactant-associated protein A, and impede the exchange of fluid between the pulmonary blood vessels and the interstitium, leading to pulmonary edema and then acute Lung damage.