寒邪致高血压大鼠脑出血的凝血-纤溶机制  

Mechanism of Thromboxane and Fibrinolysis in Hypertensive Rats with Stroke Induced by Cold Pathogens

作　　者：刘晓燕[1] 崔玉鹏[2] 李立华[1] 杨云霜[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：《安徽中医学院学报》2011年第1期51-53,共3页Journal of Anhui Traditional Chinese Medical College

基　　金：北京市自然科学基金(7072038)

摘　　要：目的研究气温骤降所形成的寒邪导致高血压大鼠发生脑卒中的凝血-纤溶机制。方法采用易卒中型肾血管性高血压(stroke prone renovascular hypertension,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凝血-纤溶标记物F1+2和D-dimer的变化。结果气温骤降形成的寒邪可以导致正常对照大鼠凝血-纤溶标志物F1+2和D-dimer水平降低。模型组大鼠F1+2水平在降温前明显高于正常对照组大鼠(P<0.05),在受到寒邪刺激时F1+2和D-dimer水平显著降低(P<0.01),降温后F1+2水平显著回升(P<0.01),D-dimer水平呈现上升趋势。结论机体凝血-纤溶活性的异常是寒邪诱发脑出血发病的重要机制之一。Objective To study the mechanism of thromboxane and fibrinolysis in hypertensive rats with stroke induced by cold pathogens caused by sudden drop of temperature.Methods The modified rat model of stroke prone renovascular hypertension（RHRSP） was employed,and stroke was induced using man-made sudden drop of temperature.The changes in plasma levels of F1＋2 and D-dimer were observed before and after the temperature drop.Results The levels of F1＋2 and D-dimer were decreased by cold pathogens caused by sudden drop of temperature in normal control rats.Before the sudden drop of temperature,the level of F1＋2 in the model group was significantly lower than that in the normal control group（P〈0.01）;the levels of F1＋2 and D-dimer were significantly decreased during the dropping stage of temperature（P〈0.01）;the level of F1＋2 was significantly increased after the drop of temperature（P〈0.01）,and the level of D-dimer showed an increasing tendency.Conclusion The abnormality in activities of thromboxane and fibrinolysis is one of the mechanisms of the onset of cerebral hemorrhage induced by cold pathogens.

关 键 词：寒邪 气温骤降 高血压 脑出血 凝血 纤溶 

分 类 号：R544.1[医药卫生—心血管疾病] R241.4[医药卫生—内科学]