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目的:研究气温骤降导致高血压大鼠发生脑卒中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降环境中诱发脑卒中,检测气温骤降前后大鼠血液流变学中全血黏度、血浆黏度、红细胞压积和红细胞聚集指数的变化。结果:气温的骤降所引起的高血压大鼠的卒中现象主要是以脑出血为主。气温的骤降使正常生理组大鼠的全血黏度、血浆黏度(P<0.01)、红细胞压积、红细胞聚集指数(P<0.05)明显降低而且相对稳定。但高血压模型大鼠则表现为:在气温骤降的初期,机体的血液流变学指标不出现下降,反而表现出不改变甚至小幅上升。但对于第2次降温后的脑出血大鼠,全血黏度(P<0.05)、血浆黏度(P<0.01)、红细胞压积(P<0.01)、红细胞聚集指数(P<0.05)则均呈现明显的大幅下降,甚至低于同一时间段的正常生理组大鼠。结论:对血液流变学调节的异常是气温骤降引起脑卒中发病的重要机制。
Objective: To study the mechanism of hemorheology in stroke caused by temperature drop in hypertensive rats. Methods: Stroke-prone renovascular hypertension (RHRSP) model was used to induce stroke in artificial simulated temperature drop environment. Whole blood viscosity, plasma viscosity, erythrocyte Changes in pressure and erythrocyte aggregation index. Results: Stroke in hypertensive rats caused by the sudden drop in temperature was mainly caused by cerebral hemorrhage. The temperature drop caused the whole blood viscosity, plasma viscosity (P <0.01), hematocrit and erythrocyte aggregation index (P <0.05) in normal physiology group decreased obviously and were relatively stable. Hypertensive rats showed the following: in the early stage of temperature drop, the body’s blood rheology indicators did not appear to decline, but showed no change or even slightly increased. However, the whole blood viscosity (P <0.05), plasma viscosity (P <0.01), hematocrit (P <0.01) and erythrocyte aggregation index (P <0.05) Significantly decreased, even lower than normal physiology rats at the same time period. CONCLUSIONS: Abnormalities in hemorheology are important mechanisms for the onset of stroke due to a sudden drop in temperature.