Ang-1、Ang-2差异表达在大鼠失血性休克血管反应性双相变化中的作用  

Differential expression of Ang-1 and Ang-2 proteins contributes to biphasic changes of vascular reactivity after hemorrhagic shock in rats

作　　者：徐竞[1] 李涛[1] 杨光明[1] 刘良明[1] 

机构地区：[1]第三军医大学大坪医院野战外科研究所二室,创伤、烧伤与复合伤国家重点实验室,重庆400042

出　　处：《中国病理生理杂志》2010年第9期1684-1688,共5页Chinese Journal of Pathophysiology

基　　金：国家自然科学基金资助项目(No30801189);重庆市自然科学基金资助项目(NoCSTC;2008BB5103)

摘　　要：目的:观察血管生成素-1(Ang-1)、血管生成素-2(Ang-2)在失血性休克后肠系膜上动脉中的表达变化,及其在失血性休克血管反应性双相变化中的作用。方法:采用离体微血管环张力测定技术和Western blotting技术,观察失血性休克后不同时点肠系膜上动脉(SMA)一级分支微血管环的血管反应性、SMA中Ang-1、Ang-2的蛋白表达变化;并观察在缺氧高血管反应期和低血管反应期,给予和抑制Ang-1、Ang-2对SMA一级分支血管环血管反应性的影响。结果:(1)失血性休克后,肠系膜上动脉血管反应性呈早期增高、晚期降低的双相变化,休克10min组NE的Emax最高,为正常的129.3%(P<0.01);Ang-1的蛋白表达也呈早期增高、晚期降低的双相变化,休克10min组的Ang-1蛋白表达最高,为正常对照组的1.85倍;Ang-2的蛋白表达在休克早期变化不大,在休克后期逐渐增高,休克4h组的Ang-2蛋白表达最高,为正常对照组的2.90倍。(2)在高血管反应期(缺氧30min),外源性给予Ang-1对血管反应性影响不大,尽管NE的Emax增大,但无显著差异(P>0.05),外源性给予Ang-2可降低血管反应性(P<0.01);在低血管反应期(缺氧4h),外源性给予Ang-1可改善血管反应性(P<0.01),外源性给予Ang-2可进一步降低血管反应性(P<0.01)。结论:失血性休克后,肠系膜上动脉存在Ang-1、Ang-2的差异表达,这种差异表达参与了失血性休克血管反应性双相变化的形成。AIM： To observe the protein expression of angiopoietin-1 （ Ang-1） and angiopoietin-2 （ Ang-2） after hemorrhagic shock,and to explore the role of this difference in the development of the biphasic change of vascu-lar reactivity after hemorrhagic shock in rats. METHODS： The vascular reactivity of the first class arborization of superior mesenteric artery （ SMA） and protein expression of Ang-1 and Ang-2 after hemorrhagic shock were measured via the iso-lated organ perfusion system and Western blotting technique. The relationship between the protein expression of Ang-1 / Ang-2 and the vascular reactivity after hemorrhagic shock was observed. By treatment with Ang-1 and Ang-2 or inhibi-tion of Ang-1 and Ang-2,the effects of angiopoietins on the vascular reactivity of SMA in the early stage （ hyperreactivi-ty） and late period （ hyporeactivity） of hypoxia were observed to analyze the role of the differential expression of Ang-1 and Ang-2 protein in the biphasic change of vascular reactivity after hemorrhagic shock. RESULTS： （ 1） The vascular reactivity of SMA showed a biphasic change following hemorrhagic shock,which was increased in the early stage of shock, and decreased in prolonged stage. The Emax of norepinephrin in the shock 10 min group was the highest （ 129. 3% of normal control,P 0. 01） . The protein expression of Ang-1 in SMA was also increased in the early stage of shock,decreased at prolonged stage of shock,and topped at 10 min shock group （ 1. 85 folds of normal control,P 0. 01） . The protein expres-sion of Ang-2 in SMA didn＇t change obviously in the early stage of shock,yet it was increased at prolonged stage of shock, and topped at 4 h shock group （ 2. 90 folds of normal control,P 0. 01） . （ 2） In the hyperreactivity stage （ hypoxia for 30 min） ,the extrinsic source of Ang-1 further increased the vascular reactivity,while the extrinsic source of Ang-2 decreased the vascular reactivity （ P 0. 01） . In the hyporeactivity stage （ hypoxia for 4 h） ,A

关 键 词：休克 出血性 血管反应性 双相变化 血管生成素-1 血管生成素-2 

分 类 号：R605.971[医药卫生—急诊医学]