Cao Chun-shui, Yin Qin, Huang Liang, Zhan Zuan, Yang Ji-bin, Xiong Hua-wei
Department of Emergency Medicine, the First Affiliated Hospital of Nanchang University, Nanchang 330006, Jiangxi, China.
Zhongguo Wei Zhong Bing Ji Jiu Yi Xue. 2010 Jul;22(7):426-9.
To investigate the effect of angiotensin II (Ang II) on the expression of aquaporin 1 (AQP1) in lung of rats with acute lung injury (ALI) and the role of Ang II in the formation of lung edema.
Forty healthy Sprague-Dawley (SD) rats were randomly divided into sham-operated group, model group, Ang II receptor blocker pretreatment group, and Ang II receptor blocker treatment group according to random digits table, with 10 rats in each group. ALI model of rats was reproduced with administration of endotoxin after hemorrhagic shock. In rats of pretreatment group Ang II receptor blocker 30 microg/kg was given 30 minutes before lipopolysaccharide (LPS) injection; rats in treatment group Ang II receptor blocker 30 microg/kg was given 30 minutes after LPS injection; rats in model group received 30 microg/kg normal saline 30 minutes before and after LPS injection. Rats were sacrificed 6 hours after model establishment, samples of venous blood and lung tissue were collected, radioimmunoassay was used to measure the level of tumor necrosis factor-alpha (TNF-alpha) in serum and the expression of Ang II in lung tissue, ratio of wet to dry (W/D) weight of lung tissue was calculated, reverse transcription-polymerase chain reaction was used to measure the expression of AQP1 mRNA in lung tissue.
Compared with rats of sham-operated group, the level of TNF-alpha in venous blood, W/D ratio and the expression of Ang II in lung tissue increased significantly, the expression of AQP1 mRNA in lung tissue decreased significantly in rats of ALI. Compared with rats of model group, the level of TNF-alpha in venous blood (microg/L) decreased significantly (4.79+/-0.24, 5.55+/-0.36 vs. 6.34+/-0.31, both P<0.05), W/D ratio decreased significantly (4.34+/-0.23, 4.85+/-0.20 vs. 5.41+/-0.26, both P<0.05), the expression of AQP1 mRNA in lung tissue increased significantly (0.854+/-0.067, 0.727+/-0.081 vs. 0.358+/-0.071, both P<0.05), and the expression of Ang II in lung tissue (ng/g) decreased to some extent (172.19+/-15.82, 202.82+/-20.47 vs. 245.88+/-26.31), but without statistical significance (both P>0.05) in rats of pretreatment group and treatment group. The expression of AQP1 mRNA was negatively correlated with both the level of Ang II and W/D ratio (r1=-0.782, r2=-0.726, both P<0.05).
During ALI, Ang II may downregulate the expression of AQP1 mRNA in lung tissue directly or through inflammatory mediators, Ang II may play a role in the formation of lung edema.
探讨血管紧张素Ⅱ（AngⅡ）对急性肺损伤（ALI）大鼠肺组织水通道蛋白1（AQP1）表达的影响以及AngⅡ在肺水肿形成中的作用。
将40只健康的Sprague-Dawley（SD）大鼠按随机数字表法随机分为假手术组、模型组、AngⅡ受体阻滞剂预处理组和AngⅡ受体阻滞剂治疗组，每组10只。采用失血性休克后注射内毒素的方法复制大鼠ALI模型。预处理组大鼠在注射脂多糖（LPS）前30分钟给予AngⅡ受体阻滞剂30μg/kg；治疗组大鼠在注射LPS后30分钟给予AngⅡ受体阻滞剂30μg/kg；模型组大鼠在注射LPS前后30分钟均给予30μg/kg生理盐水。造模后6小时处死大鼠，采集静脉血和肺组织样本，采用放射免疫法检测血清肿瘤坏死因子-α（TNF-α）水平和肺组织中AngⅡ的表达，计算肺组织湿/干（W/D）重量比，采用逆转录-聚合酶链反应检测肺组织中AQP1 mRNA的表达。
与假手术组大鼠相比，ALI大鼠静脉血中TNF-α水平、W/D比值及肺组织中AngⅡ表达显著升高，肺组织中AQP1 mRNA表达显著降低。与模型组大鼠相比，预处理组和治疗组大鼠静脉血中TNF-α水平（μg/L）显著降低（4.79±0.24，5.55±0.36比6.34±0.31，P均<0.05），W/D比值显著降低（4.34±0.23，4.85±0.20比5.41±0.26，P均<0.05），肺组织中AQP1 mRNA表达显著升高（0.85±0.067，0.72±0.081比0.35±0.071，P均<0.05），肺组织中AngⅡ表达（ng/g）有一定程度降低（172.19±15.82，202.82±20.47比245.88±26.31），但差异无统计学意义（P均>0.05）。AQP1 mRNA表达与AngⅡ水平和W/D比值均呈负相关（r1=-0.782，r2=-0.726，P均<0.05）。
在ALI过程中，AngⅡ可能直接或通过炎症介质下调肺组织中AQP1 mRNA的表达，AngⅡ可能在肺水肿形成中起作用。
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