高温诱发脑梗塞发病的凝血纤溶活性机制研究  

The Mechanism Study of Thromboxane and Fibrinolysis in Hypertensive Rats with Infarction Induced by High Temperature

作　　者：刘晓燕[1] 崔玉鹏[2] 郭霞珍[1] 李立华[1] 

机构地区：[1]北京中医药大学基础医学院,北京100029 [2]首都体育学院,北京100088

出　　处：《中华中医药学刊》2011年第6期1349-1350,共2页Chinese Archives of Traditional Chinese Medicine

基　　金：北京市自然科学基金资助项目(7072038)

摘　　要：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 mechanism of thromboxane and fibrinolysis in hypertensive rats with infarction induced by sudden high temperature.Methods Adopt the improved rats model of strokes prone renovascular hypertensive（RHRSP）,then were carried out in man-made sudden high temperature to induce infarction.To detect the changes F1＋2 and D-dimer before and after the temperature rise.Results high temperature increased the level of F1＋2 and decreased the level of D-dimer in the normal rats.It is lower than normal rats when the hypertensive rats are at normal temperature（P0.05）.Moreover,the level of F1＋2 and D-dimer changes abnormally in the infarction rats when the temperature rised,F1＋2 rised and D-dimer dropped..Conclusion It is the important mechanism of infarction induced by high temperature that the body modulates the thromboxane and fibrinolysis abnormally.

关 键 词：高温 气温骤升 高血压 凝血纤溶 脑梗塞 

分 类 号：R473.71[医药卫生—护理学]