火热邪气诱发高血压大鼠脑梗死发病血管活性机制的研究  

Vasoactive Mechanism of Cerebral Infarction on Hypertensive Rats Induced by Hot Pathogens

作　　者：刘晓燕[1] 李立华[1] 杨云霜[1] 郭霞珍[1] 

机构地区：[1]北京中医药大学基础医学院,北京100029

出　　处：《吉林中医药》2013年第9期925-928,共4页Jilin Journal of Chinese Medicine

基　　金：国家中医药管理局中医基础理论重点学科;北京市自然科学基金项目(7072038)

摘　　要：目的研究火热邪气导致高血压大鼠发生脑梗死的机制。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环境中诱发脑梗死,检测气温骤升刺激前后大鼠ET-1、AngⅡ、AVP和NO水平的变化。结果骤然升温使生理组和模型组大鼠缩血管因子ET-1、AngⅡ和AVP水平均降低,生理组AVP变化明显(P<0.01)。升温结束后生理组大鼠ET-1、AngⅡ和NO水平均较升温中和升温前明显升高(P<0.01或P<0.05)。但高血压模型组大鼠,升温中缩血管物质ET-1、AngⅡ和AVP变化不明显,而舒张血管的NO却明显升高(P<0.01)。升温结束后,模型组发生脑梗死大鼠的ET-1、AngⅡ和AVP水平均较升温前和升温中变化不明显,但NO水平却持续升高,明显高于模型组升温前和生理组升温后水平(P<0.01)。结论高血压状态下血管收缩反应性降低,舒张反应性异常增高,血管舒缩调节紊乱,此为火热邪气促发脑梗死发病的重要发病机理。Objective To study the mechanism of hypertensive rats with infarction induced by hot pathogens caused by sud- den rising of temperature. Methods The rat of stroke prone renovascular hypertensive （RHRSP）was used, and stroke was induced using man-made sudden rising of temperature. The changes in blood levels of ET-1 ,Ang Ⅱ ,AVP and NO were ob- served before and after the temperature rises. Results The levels of ET-1, Ang n and AVP were decreased on the sudden rising of temperature in the normal groups and the model groups, especially the level of AVP in the normal group changed significantly（ P 〈 0.01）. After rising of temperature, the levels of ET-1 ,Ang ⅡI and NO in the normal groups were higher significantly than those before rising temperature and those on the rising temperature（ P 〈 0.01 or P 〈 0.05）. However, to the model groups, the levels of ET- 1, AngⅡ and AVP on the rising of temperature were not changed significantly, but the level of NO rose significantly（ P 〈 0.01）. After the sudden rising temperature, the levels of ET-1 ,AngⅡ and AVP of the model rats with cerebral infarction did not change significantly comparing with those before rising temperature and those on the rising temperature. However the level of NO rose continuously, even was higher than that before rising temperature of model group, and that after rising temperature of normal group （ P 〈 0. 01 ）. Conclusion The decrease of vasoconstriction reactive and the abnormal increase of vasodilator response in the hypertension status are the important mechanisms of infarc- tion induced by hot pathogens.

关 键 词：火邪 气温骤升 高血压 脑梗死 发病机制 

分 类 号：R473.1[医药卫生—护理学]