摘要
目的观察金钠多对急性缺氧、血管紧张素Ⅱ(AngⅡ)及两者联合作用条件下血管内皮细胞(VEC)的保护作用。方法将培养的血管内皮细胞分为7个组:1)对照组;2)单纯缺氧组;3)缺氧+金钠多组;4)单纯血管紧张素Ⅱ组;5)血管紧张素Ⅱ+金钠多组;6)缺氧+血管紧张素Ⅱ组;7)缺氧+血管紧张素Ⅱ+金钠多组。有缺氧因素的各组均置于低压舱内上升至5 000 m高度、停留30 m in,对培养的各组血管内皮细胞进行缺氧。用放射免疫法测定缺氧及血管紧张素Ⅱ和金钠多作用前、作用后0.5h、6.0 h、24.0 h各组细胞培养液中的内皮素含量。结果1)单纯缺氧和单纯血管紧张素Ⅱ均可明显促进血管内皮细胞分泌内皮素(P<0.01);2)在缺氧和血管紧张素-Ⅱ联合作用下促血管内皮细胞分泌内皮素的作用高于单纯缺氧组和单纯血管紧张素Ⅱ组(P<0.01);3)金钠多能显著降低单纯缺氧、单纯血管紧张素Ⅱ及缺氧加血管紧张素Ⅱ条件下血管内皮细胞分泌的内皮素含量。结论1)在单纯缺氧、单纯血管紧张素Ⅱ及两者联合作用条件下均可显著增加血管内皮细胞分泌内皮素的功能;2)金钠多对单纯缺氧、单纯血管紧张素Ⅱ及两者联合作用条件下血管内皮细胞均有明显的保护作用。
Objective To observe the protection of Ginaton on vascular endothelial cells(VEC) secreting endothelia(ET) induced with hypoxia,Ang Ⅱ or hypoxia combined Ang Ⅱ. Methods Cultured VEC were divided into 7 groups : 1 ) control group ;2) simple hypoxia group ;3 ) hypoxia + Ginaton group ;4) simple Ang Ⅱ group ; 5) Ang Ⅱ group + Ginaton group; 6) hypoxia + Ang Ⅱ group; 7 ) hypoxia + Ang Ⅱ + Ginaton group. All groups induced with hypoxia were put in a hypobaric chamber at the altitude of 5 000 m for 30 rain to make hypoxia factor. The ET content in supernatant of VEC were measured with radioimmunoassay at 0 h, 0.5 h, 6.0 h and 24.0 h. Results 1 ) Simple hypoxia or simple Ang Ⅱ promoted the VEC secreting ET significantly (P 〈0. 01 ) ;2) The ET release of VEC induced by hypoxia + Ang Ⅱ was significant more than simple hypoxia or simple Ang Ⅱ (P 〈0.01 ) ;3) Ginaton had the effect to inhibit the VEC secreting ET induced by hypoxia,Ang Ⅱ or hypoxia combined Ang Ⅱ (P 〈0.01 ). Conclusion 1 ) Hypoxia,Ang Ⅱ or hypoxia combined Ang Ⅱ can significantly increase the ET release of VEC ;2) Ginaton has the protective function to decrease the VEC secreting ET induced by hypoxia,Ang Ⅱ or hypoxia combined Ang Ⅱ.
出处
《航天医学与医学工程》
CAS
CSCD
北大核心
2009年第2期94-97,共4页
Space Medicine & Medical Engineering
基金
海军后勤医学科研基金项目(00-3321)