冷应激高血压大鼠血管舒缩功能的研究

Vascular Function in Cold Stress Induced Hypertensive Rats

目的 探讨寒冷环境因素在大鼠高血压发病中的作用。方法 40只 3月龄雄性Wistar大鼠 ,随机分成寒冷组和对照组 ,寒冷组动物置于 4± 2℃的冷环境中 ,每天 4小时 ,共 8周。每周测鼠尾血压、心率、体重。 8周后取胸主动脉完整血管环 ,生理多导记录仪分析血管活性物质对离体血管环舒缩功能的影响。结果 寒冷组的鼠尾压、心率均明显升高 (P <0 0 1 ) ,四周鼠尾血压达到最高 (为 1 36 .4± 5 .5mmHg)。血管环功能实验表明 ,冷应激组大鼠血管环对AngⅡ、NE、NTG的反应性与正常组无差别 ,但对钙通道开放剂 (Bayk 8644)的收缩反应明显增强 (P <0 0 1 )及Ach引起的内皮依赖的舒张反应明显减弱 (P <0 0 5)。结论 冷应激环境因素刺激可导致大鼠高血压和血管功能异常 。

Objective To investigate the role of cold stress in the development and maintenance of hypertension. Methods 3 month old Wistar rats were randomly divided into two groups: (1)Cold stress group(C, n =20): Rats were exposed to cold (4±2℃) for 4 hours per day for 8 weeks; (2)Control group (N, n =20). Systolic blood pressure (SBP) and heart rate were measured weekly by tail cuff technique. Isometric force of aortic ring was measured using a force transducer. Results SBP and heart rate in cold stress rats were significantly increased ( P <0 01) than that nomal rats during the whole experiment. Blood pressure reached peak level on 4th week in cold stress rats (136.4±5.5 mmHg ). Reactivity of aortic ring stimulated by NE?AngⅡ and NTG remain no differences between cold and normal group, but the contraction of aortic ring stimulated by Bayk 8644 was significantly increased ( P <0 01) and vasorelaxation stimulated by Ach was significantly decreased ( P <0 05) in cold stress rats. Conclusions Cold stress plays an important role in the development of hypertensive and vascular dysfunctions. The mechanism may be involved in openity or activationof calcium channels and reduced endothelium depended vasorelaxation.