“失血性休克-内毒素”二次打击所致肺损伤水通道蛋白的表达  

Expression of aquaporin-1 and aquaporin-5 in uncontrolled hemorrhagic shock induced acute lung injury in a two-hit model in rats

作　　者：高巨[1] 招伟贤[1] 肖建斌[1] 徐少群[1] 石永勇[1] 

机构地区：[1]广州中医药大学第二附属医院(广东省中医院)麻醉科,510120

出　　处：《中国急救医学》2007年第6期546-549,共4页Chinese Journal of Critical Care Medicine

基　　金：广东省医学科研基金资助项目(No.A2005269);广东省中医药管理局资助项目(No.2050069)

摘　　要：目的探讨水通道蛋白(AQP)-1和AQP-5在失血性休克-内毒素二次打击所致大鼠肺损伤中的表达。方法30只SD大鼠随机分为两组:假手术对照组(C组)、二次打击组(HS组),每组15只。建立“未控制性失血性休克-内毒素”二次打击大鼠模型,并按院前期90min、院内复苏期60min、院内观察期三期进行实验。实验结束前采血测动脉血气并比较两组大鼠存活率。测定肺泡灌洗液蛋白(BALFpro)、肺通透指数(PPI)及肺组织湿/干质量比(W/D);HE染色光镜下观察肺损伤程度;采用免疫组化法分别测定肺组织AQP-1和AQP-5的蛋白表达。结果与C组比较,HS组MAP、lac、PaO2、pH、BE、PPI、BALFpro、W/D等指标均明显恶化,肺组织损伤严重,大鼠存活率降低;与C组比较,HS组肺组织AQP-1和AQP-5的表达显著降低(P<0.01)。结论二次打击所致大鼠肺损伤时AQP-1和AQP-5表达均明显降低,这可能是失血性休克后肺损伤肺水肿形成的重要原因之一。Objective To investigate the expression of aquaporin - 1 （ AQP - 1 ） and aquaporin - 5 （ AQP - 5 ） in hemorrhagic shock induced acute lung injury in a two - hit model of hemorrhagic shock followed by mimicked infection. Methods Thirty SD rats were randomly assigned to the following two groups： control group （ C group, surgery, no hemorrhage, and no resuscitation ） , two - hit model group （ HS group）. We used three -phased uncontrolled hemorrhagic shock model in rats. Hemorrhagic shock phase I began with blood withdrawal over 15 min, animals were subjected to massive hemorrhage [ mean arterial pressure （MAP）= 35 -40 mm Hg for 60 min and followed by intratracheal lipopolysaccharide 2 mg/kg （ two - hit model ）. At hemorrhagic shock 90 min, resuscitation phase Ⅱ of 60 min began with hemostasis, return of all the blood initially shed, plus fluids. Observation phase Ⅲ was to 3.5 h. After phase Ⅲ, arterial blood gas and survival rates were recorded. Lung tissue was sampled to measure values of wet - to - dry lung weight ratio （ W/D ） , pulmonary permeability index （ PPI ） , BALF protein, and immunohistochemical used for detection of expression of AQP - 1 and AQP - 5. Results Compared with the C group, the HS group significantly decreased survival rates and increased pulmonary microvascular permeability and wet - to - dry lung weight ratio, and also decreased the AQP1 and AQP5 expression in lung tissue. Conclusions These findings showed that the expression of AQP1 and AQP5 may play an important role in abnormal fluid transportation and formation of pulmonary edema in uncontrolled hemorrhagic shock - induced ALI.

关 键 词：失血性休克 肺损伤 水通道蛋白-1 水通道蛋白-5 

分 类 号：R459.7[医药卫生—急诊医学] R563.8[医药卫生—治疗学]