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目的:研究气温骤升所形成的高温导致高血压大鼠发生脑梗塞的凝血-纤溶活性机制。方法:采用易卒中型肾血管性高血压(RHRSP)模型,放置于人工模拟气温骤升的高温环境中诱发脑梗塞,检测高温刺激前后大鼠凝血-纤溶标记物F1+2和D-d im er的变化。结果:高温可以导致正常生理大鼠F1+2升高,D-d im er下降,且F1+2水平可在高温结束后恢复。高血压大鼠在未受高温刺激时F1+2和D-d im er(P<0.01)水平均低于正常生理组大鼠,在受到高温刺激时F1+2和D-d im er的波动呈现异常,表现为F1+2含量持续升高,而D-d im er的含量则下降。结论:机体对凝血-纤溶系统调节的异常是高温诱发脑梗塞发病的重要机制之一。
OBJECTIVE: To study the coagulation-fibrinolytic mechanism of cerebral infarction in hypertensive rats induced by the high temperature caused by the sudden warming of temperature. Methods: Stroke-prone renovascular hypertension (RHRSP) model was used to induce cerebral infarction in a simulated high temperature environment. The coagulation-fibrinolysis markers F1 + 2 and Ddim er The change. Results: High temperature could lead to the increase of F1 + 2 and D-d im er in normal rats, and the level of F1 + 2 could recover after the end of high temperature. The levels of F1 + 2 and Dd im er (P <0.01) in hypertensive rats were lower than those in normal rats when stimulated by high temperature, and the fluctuations of F1 + 2 and Dd im er were abnormal when stimulated by high temperature F1 + 2 content continued to rise, while the Dd im er content decreased. Conclusion: Abnormal regulation of coagulation - fibrinolysis system is one of the important mechanisms of high temperature induced cerebral infarction.