摘要
目的:研究气温骤升诱发高血压大鼠发生脑梗塞血液流变学的相关机制。方法:采用改良的黄如训方法复制大鼠易卒中型肾血管性高血压(RHRSP)模型,放置于人工模拟的气温骤升环境中诱发脑梗塞,检测气温骤升前后大鼠血液流变学中全血黏度、红细胞聚集和电泳指数。结果:气温骤升时,所有大鼠全血黏度、红细胞聚集和电泳指数指标均升高,模型组变化幅度最大;升温结束后,生理组、伪手术组全血黏度下降,而模型组仍呈上升趋势(P<0.05或P<0.01),而且模型组升温后的全血黏度、红细胞聚集和电泳指数均明显高于同时间点生理组和伪手术组(P<0.05或P<0.01)。结论:气温骤升会导致机体血液流变学的波动,自我恢复能力下降,血液黏度变化幅度大和持续时间长是气温突升诱发存在高血压基础病变发生脑梗塞的重要机制。
Objective： To study the mechanism of hemorheology in hypertensive rats with cerebral infarction induced by sudden rising of temperature. Methods： Rats models of strokes prone to renovascular hypertensive （RHRSP） were established by the improved Huang Ruxun and were put in man-made sudden rising of temperature to induce cerebral infarction. Detect the changes of the blood viscosity, erythrocyte aggregation and electrophoresis before and after temperature rising.Results：The blood viscosity, erythrocyte aggregation and electrophoresis of all rats were heightened by sudden rising of temperature, having the largest range ability in the model group; when the temperature stopped rising, the blood viscosity of rats in normal group and sham-operated group descended, but the model group was still ascending （P 〈 0.05 or P 〈 0.01）. Moreover, the three indexes of model group of cerebral infarction rats were higher than those of normal and sham-operated rats at the same time after rising temperature （P 〈 0.05 or P 〈 0.01）. Conclusions：Sudden rising of temperature leads hemorheology to fluctuate, resulting in a poor recovery capability. The large range ability and long persistence time of the blood viscosity to change was an important mechanism of hypertensive organism with induced cerebral infarction.
出处
《现代生物医学进展》
CAS
2009年第7期1224-1226,1229,共4页
Progress in Modern Biomedicine
基金
北京市自然科学基金项目资助(NO.7072038)。
关键词
气温骤升
高血压
脑梗塞
血液流变学
Sudden rising of temperature
Hypertension
Cerebral infarction
Hemorheology
