上皮钠通道在高氧致新生大鼠支气管肺发育不良早期肺水肿发生中的作用

The role of epithefial sodium channel in the neonatal rat bronchopulmonary dysplasia early pulmonary edema induced by hyperoxia

目的探讨高氧致新生大鼠肺水肿阶段上皮钠通道（ENaC）蛋白表达及钠水转运功能的变化。方法将新生大鼠随机分成高氧组和空气组，于实验后1、3、5、7d收集肺组织，计算肺湿、干质量比率以确定血管外肺水含量变化，应用Westernblot方法检测高氧暴露后新生大鼠肺组织ENaC3个主要亚基（α，β和γ）蛋白表达的变化规律。检测实验后5d肺泡液体清除率（AFC）及阿米洛利敏感性AFC的变化。结果高氧暴露后新生大鼠肺组织血管外肺水含量增加（肺湿、干质量比率：3d：6．37±0．64与5．56±0．15，t=3．46；5d：5．86±0．52与5．11±0．21，t=-3．82；7d：5．56±0．45与4．80-4-0．09，t：-4．72；P均〈0．01），而AFC显著增加，阿米洛利非敏感性AFC无显著改变[AFC：（20．32±3．33）％与（12．97±2．46）％，t=-6．16，P〈0．01；阿米洛利非敏感性AFC：（10．42±3．44）％与（8．67±3．13）％，t=-1．30，P=0．21]，高氧暴露使阿米洛利敏感性AFC增加；仪，p和1-ENaC蛋白表达在高氧暴露后与空气组比较并无减低。结论虽然在高氧诱导的支气管肺发育不良早期发生了肺水肿，但ENaC钠水主动转运障碍并非引起高氧暴露后肺水肿发生的主要因素。

Objective To investigate the changes of epithelial sodium channel（ENaC） expression and sodium and water transport function in the neonatal rat pulmonary edema induced by hyperoxia. Methods The neonatal rats were randomly divided into the hyperoxia group and the control group. After 1,3,5 and 7 d hyperoxia exposure, the lung tissues were collected to measure the wet-to-dry weight ratio and the expression of α-, β- and γ-ENaC subunits were detected by western blot analysis. Alveolar fluid clearance （AFC） and amiloride-sensitive AFC were measured after 5 d to reveal the effect of hyperoxia on the activity of ENaC. Results The lung water contents significantly increased in the hyperoxia group indicating that pulmonary edema happened（3 d：（6. 37±0.64） vs （5.56±0. 15）,t =3.46,P 〈0.01;5 d：（5.86±0.52） vs （5.11 ＋0.21）, t= - 3.82,P 〈0.01;7 d： （5.56 ±0.45） vs （4.80± 0. 09）,t = -4.72,P 〈 0.01）.AFC increased significantly, but no significant difference was found in amiloride-insensitive AFC between the two groups which indicate that amiloride-sensitive AFC increased significantly （ AFC ： （ 20. 32± 3.33 ） % vs （ 12. 97 -＋ 2. 46 ） % , t= -6.16,P〈0.01;amiloride-insensitive AFC：（10.42±3.44）% vs （8.67 ±3.13）%,t = -1.30 P= O. 21 ）. The expression of α-, β- and γ-ENaC did not reduced after hyperoxia exposure compared with the control group. Conclusion Although bronchopulmonary dysplasia of early pulmonary edema induced by hyperoxia, dysfunctional transport of Na＋ may not be a key factor involved in pulmonary edema at the early stage of bronchopulmonary dysplasia.