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目的基于天人相应的理论,探讨气温骤升致高血压大鼠发生脑梗塞血液流变学的相关机制。方法采用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指标。结果气温骤升时,所有大鼠全血黏度、红细胞聚集、红细胞电泳指数、红细胞压积和红细胞刚性指数均升高,模型组变化幅度最大;升温结束后,生理组、假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、红细胞聚集指数、红细胞电泳指数和红细胞刚性均明显高于同时间点生理组和假手术组(P<0.05或P<0.01)。结论气温突升导致脑梗塞的发生并不在于升温能导致机体全血黏度的升高,流动性减慢,更在于以高血压为主的长期的病理基础破坏了机体适应环境变化的自我调节能力,使其在高温刺激后血液黏度持续升高而无法恢复正常的生理状态。
OBJECTIVE Based on the corresponding theory of heaven and man, this paper explores the relevant mechanisms of cerebral infarction hemorheology induced by the temperature swell in hypertensive rats. Methods Stroke-prone renovascular hypertension (RHRSP) model was used to induce cerebral infarction in artificial simulated temperature-rising environment. The hemorrheological indexes in rats before and after the temperature swell were measured. Results When the temperature was rising, the whole blood viscosity, erythrocyte aggregation, erythrocyte electrophoresis index, hematocrit and erythrocyte rigidity index of all the rats increased, and the change range of the model group was the largest. After the warming, the whole blood viscosity of the physiological group and sham operation group (P <0.05 or P <0.01), and the whole blood viscosity, erythrocyte aggregation index, erythrocyte electrophoresis index and erythrocyte rigidity of the model group were significantly higher than those of the physiological group and the false Surgery group (P <0.05 or P <0.01). Conclusions The sudden increase of temperature causes cerebral infarction to occur not because the warming can lead to the increase of the whole blood viscosity, and the fluidity slows down, but also the long-term pathological basis mainly of hypertension disrupts the self-regulating ability of the body to adapt to environmental changes , So that after high-temperature stimulation of blood viscosity continued to rise and can not return to normal physiological state.