摘要
目的探讨重度失血性休克期阻断缝隙连接对缺血性肺损伤水通道蛋白表达的影响。方法健康家兔24只，体重1．5～2．2kg，按照Wiggers改良法制作重度失血性休克模型，随机分为传统治疗组（A组）和辛醇组（B组）2组，每组12只。A组静脉输注乳酸钠林格氏液1．5ml／kg·min共30min；B组静脉输注乳酸钠林格氏液1．5ml／kg·min共30min，同时腹腔注射99．5％的辛醇5mmol／kg，然后两组回输全部放血及等放血量的乳酸钠林格氏液后再静脉输注乳酸钠林格氏液2．5ml／kg·h共150min。于放血前（T1）、失血性休克模型制备成功后即刻（T2）、容量复苏30min（T3）、容量复苏180min（T4）时记录MAP、HR，记录容量复苏期间兔的病死情况。于实验兔容量复苏死亡或复苏结束时处死后即刻取肺组织免疫组化检测Cx43及AQP1、AQP5蛋白的表达水平。结果①免疫组化Cx43的表达比较：A组每高倍镜阳性表达的细胞数较B组显著增加（P〈o．01）。②免疫组化APQ1的表达：A组每高倍镜阳性表达细胞数较B组显著减少（P〈0．01）。③免疫组化APQ5的表达：A组每高倍镜阳性表达细胞数较B组显著减少（P〈0．01）。各组内Cx43免疫组化每高倍镜阳性细胞数与AQP1、AQP5免疫组化每高倍镜阳性细胞数呈负相关。结论兔失血性休克诱发肺损伤时水通道蛋白表达增加。阻断缝隙连接可抑制肺水通道蛋白的表达，缝隙连接在水通道蛋白的表达中具有重要作用。
Objetive To investigate the effects of AQPs by blocking intercellular gap junction in lung injury in- duced by hemorrhagic shock-volume resuscitation in rabbits. Methods 24 healthy rabbits of both sexes weighing 1.5-2.2 kg were used in this study. The animals were anesthetized with iv 3 % pentobarbital 30 mg/kg, tracheostomized and me- chanically ventilated. Femoral artery was cannulated for MAP monitoring, blood-letting, blood sampling and fluid infu- sion. Severe hemorrhagic shock was induced according to the method described by Wiggers. MAP was maintained at 35- 40 mm Hg for 60 min. The animals were then randomly divided into 2 groups （n=12 each） ： traditional treatment group （group A） and octanol group （group B）. Both groups received rapid iv infusion of lactated Ringer＇s solution （LR solu- tion） 1.5 ml/kg ·min. In group B 99.5% octanol （a specific gap junction inhibitor） 5 mmol/kg was injected intraperito- neally （IP） in addition to iv LR solution infusion. Thirty minutes later the animals were resuscitated with infusion of the blood withdrawn and LR solution （the volume was equal to the volume of blood loss）. Then LR solution was infused iv at 2.5 ml/kg · h for 150 min. Left ventricular systolic pressure （LVSP）, MAP and HR were recorded before blood letting （T1）, immediately after successful establishment of the model （T2）, and at 30 and 180 min （T3-4） of resuscitation. The mortality during resuscitation was calculated. The animals were killed at the end of resuscitation. Results As compared to the immunohistochemistry in group A, the expression of Cx43 was significantly decreased in group B （P〈0.01）. As compared to the immunohistochemistry in group A, the expression of AQP1 was significantly inceased in group B. Ascompared to the immunohistochemistry in group A, the expression of AQP5 was significantly increased in group B （P〈 0.01）. There was negative correlation between Cx43 expression and AQP1 and AQP5 expression. Conclusion These re- sults indicate that the expression of AQPs are increased during the hemorrhagic shock with lung injury. The expression of AQPs is inhibited by blocking intercellular gap junction.
出处
《西部医学》
2015年第12期1772-1775,共4页
Medical Journal of West China
基金
贵州省优秀科技教育人才省长专项基金(2005305)
关键词
缝隙连接
失血性休克
肺损伤
水通道蛋白
Gap junctions
Shock, hemorrhagic
Respiratory distress syndrome, adult
AQPs
