升温诱发高血压大鼠脑梗塞发病的神经内分泌机制  

Study on Neuroendocrine Mechanism of Occurrence of Cerebral Infarction in Hypertensive Rats Induced by Soaring Temperature

作　　者：刘晓燕[1] 崔玉鹏[2] 杨云霜[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：《现代生物医学进展》2011年第8期1428-1431,共4页Progress in Modern Biomedicine

基　　金：北京市自然科学基金项目资助(NO.7072038)

摘　　要：目的:研究气温骤升导致高血压大鼠发生脑梗塞的神经内分泌机制。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ACTH、CORT、TSH、T3、T4的变化。结果:突然升温使生理组大鼠ACTH和CORT水平表现升高的趋势。模型组高血压大鼠CORT、TSH、T3、T4水平在升温中均呈现升高趋势,但是ACTH水平却明显降低(P<0.05)。升温后发生脑梗塞大鼠的ACTH和T4水平与升温前比明显下降(P<0.01),而TSH水平明显高于升温前水平(P<0.05),T3水平不变。结论:高血压机体应激反应系统紊乱,甲状腺刺激素和肾上腺皮质激素的异常波动,是突然高温促发高血压机体脑梗塞发病的重要神经内分泌机制。Objective： To investigate the neuroendocrine mechanism of sudden rising temperature on hypertensive rats with infarction..Methods： The improved rats model of strokes prone renovascular hypertensive（RHRSP） were put in man-made sudden high temperature to induce infarction.The ACTH,CORT,TSH,T3 and T4 were detected.Results： Sudden rising temperature increased the ACTH and CORT in the rats of normal groups.In the model groups,the CORT,TSH,T3 and T4 increased when the temperature rised,but the ACTH decreased（P0.05）.The ACTH and T4 decreased significantly（P0.01）,the TSH increased（P0.05）,while the level of T3 was unchanged in the rats with infarction after rising temperature than that in the rats before rising temperature,.Conclusion： The important mechanisms of infarction induced by high temperature are the disorder of alarm reaction in the hypertension body and the abnormal changes of hormones of thyroid gland and adrenal cortex.

关 键 词：气温骤升 高血压 脑梗塞 甲状腺轴 肾上腺轴 

分 类 号：Q95-3[生物学—动物学] R743[医药卫生—神经病学与精神病学]