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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 cerebral infarction induced by temperature swell in hypertensive rats. Methods: The rat model of stroke-prone renovascular hypertension (RHRSP) was reproduced by a modified Huang Ru-Xun method. The rats were placed in artificial simulated temperature-rising environment to induce cerebral infarction. The changes of whole blood rheology Blood viscosity, erythrocyte aggregation and electrophoretic index. Results: During the temperature swell, whole blood viscosity, erythrocyte aggregation and electrophoresis index of all rats were increased, and the change range of the model group was the largest. After the warming, the whole blood viscosity of the physiological group and the pseudo-surgery group decreased, while the model group was still (P <0.05 or P <0.01), and the whole blood viscosity, erythrocyte aggregation and electrophoresis index of the model group after warm-up were significantly higher than those of the physiological and sham operation groups at the same time point (P <0.05 or P <0.01). CONCLUSIONS: A sudden increase in temperature will lead to fluctuations in blood rheology, decrease in self-recovery, large changes in blood viscosity and prolonged duration, which are important mechanisms for sudden onset of cerebral infarction due to sudden temperature increase.