【摘要】 目的观察雾化吸入氟化碳(perfluorocarbon,PFC)对急性肺损伤(acute lung injury,ALI)大鼠肺水肿、肺内水通道蛋白-1(AQP-1)及钠钾ATP酶活性的影响。方法大鼠腹腔注射脂多糖(lipopolysaccharide,LPS)建立ALI模型并雾化吸入PFC进行干预。在LPS注射后6h观察PFC对ALI大鼠动脉血气、肺损伤评分、肺湿干质量比值、肺泡通透指数及钠钾ATP酶活性等的影响,并采用western-blot观察肺内AQP-1表达的变化。结果LPS性肺损伤以肺水肿为主要表现之一。雾化吸入PFC可以缓解LPS诱导ALI后的低氧血症,降低ALI大鼠的肺损伤评分、肺湿干质量比值、肺泡通透指数,同时增加肺组织钠钾ATP酶活性及AQP-1的表达。结论雾化吸入PFC减轻LPS性肺损伤大鼠肺水肿,上调肺损伤期间钠钾ATP酶活性与AQP-1表达。更多还原

【Abstract】 Objective To investigate the effects of perfluorocarbon aerosol inhalation on pulmonary edema,Na +-K+ ATPase activity and aquaporins-1 expression in rats of acute lung injury (ALI). Methods ALI was induced by intraperitoneal injection of lipopolysaccharide (LPS). 6 hours after LPS injection,artery blood gas was analyzed. Also,lung samples were collected for histopathological examination,lung injury score,wet to dry ratio,lung permeability index and Na +-K + ATPase activity analysis. Western blot method was used to determine the protein level of aquaporins-1 (AQP-1) in the lung tissues. Results LPS injection resulted in pulmonary edema,hypoxemia,lower pulmonary Na+-K+ ATPase activity and aquaporins-1 level. Perfluorocarbon aerosol inhalation reversed these effects with the decreases in lung injury score,wet to dry ratio and lung permeability index. Conclusion Perfluorocarbon aerosol inhalation attenuates LPS-induced pulmonary edema,which possibly contributes to its abilities to increase pulmonary Na +-K + ATPase activity and aquaporins -1 level in LPS-treated rats.更多还原