中国综合临床
中國綜閤臨床
중국종합림상
CLINICAL MEDICINE OF CHINA
2013年
2期
204-208
,共5页
高氧%肺水肿%新生大鼠%上皮钠通道
高氧%肺水腫%新生大鼠%上皮鈉通道
고양%폐수종%신생대서%상피납통도
Hyperoxia%Pulmonary edema%Neonatal rat%Epithelial sodium channel
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Western blot方法检测高氧暴露后新生大鼠肺组织ENaC 3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:3 d:6.37±0.64与5.56±0.15,=3.46;5 d:5.86±0.52与5.11±0.21,t=-3.82;7 d:5.56±0.45与4.80±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；α,β和γ-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.
目的 探討高氧緻新生大鼠肺水腫階段上皮鈉通道(ENaC)蛋白錶達及鈉水轉運功能的變化.方法 將新生大鼠隨機分成高氧組和空氣組,于實驗後1、3、5、7d收集肺組織,計算肺濕、榦質量比率以確定血管外肺水含量變化,應用Western blot方法檢測高氧暴露後新生大鼠肺組織ENaC 3箇主要亞基(α,β和γ)蛋白錶達的變化規律.檢測實驗後5d肺泡液體清除率(AFC)及阿米洛利敏感性AFC的變化.結果 高氧暴露後新生大鼠肺組織血管外肺水含量增加(肺濕、榦質量比率:3 d:6.37±0.64與5.56±0.15,=3.46;5 d:5.86±0.52與5.11±0.21,t=-3.82;7 d:5.56±0.45與4.80±0.09,t=-4.72;P均＜0.01),而AFC顯著增加,阿米洛利非敏感性AFC無顯著改變[AFC:(20.32±3.33)％與(12.97±2.46)％,t=-6.16,P＜0.01；阿米洛利非敏感性AFC:(10.42±3.44)％與(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；α,β和γ-ENaC蛋白錶達在高氧 暴露後與空氣組比較併無減低.結論 雖然在高氧誘導的支氣管肺髮育不良早期髮生瞭肺水腫,但ENaC鈉水主動轉運障礙併非引起高氧暴露後肺水腫髮生的主要因素.
목적 탐토고양치신생대서폐수종계단상피납통도(ENaC)단백표체급납수전운공능적변화.방법 장신생대서수궤분성고양조화공기조,우실험후1、3、5、7d수집폐조직,계산폐습、간질량비솔이학정혈관외폐수함량변화,응용Western blot방법검측고양폭로후신생대서폐조직ENaC 3개주요아기(α,β화γ)단백표체적변화규률.검측실험후5d폐포액체청제솔(AFC)급아미락리민감성AFC적변화.결과 고양폭로후신생대서폐조직혈관외폐수함량증가(폐습、간질량비솔:3 d:6.37±0.64여5.56±0.15,=3.46;5 d:5.86±0.52여5.11±0.21,t=-3.82;7 d:5.56±0.45여4.80±0.09,t=-4.72;P균＜0.01),이AFC현저증가,아미락리비민감성AFC무현저개변[AFC:(20.32±3.33)％여(12.97±2.46)％,t=-6.16,P＜0.01；아미락리비민감성AFC:(10.42±3.44)％여(8.67±3.13)％,t=-1.30,P=0.21],고양폭로사아미락리민감성AFC증가；α,β화γ-ENaC단백표체재고양 폭로후여공기조비교병무감저.결론 수연재고양유도적지기관폐발육불량조기발생료폐수종,단ENaC납수주동전운장애병비인기고양폭로후폐수종발생적주요인소.
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 edemahappened(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 =0.21).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.
