刘晓燕1△ 崔玉鹏2 杨云霜1 李立华1.升温诱发高血压大鼠脑梗塞发病的神经内分泌机制[J].现代生物医学进展英文版,2011,11(8):1428-1431. |
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 Infarctionin Hypertensive Rats Induced by Soaring Temperature |
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DOI: |
中文关键词: 气温骤升 高血压 脑梗塞 甲状腺轴 肾上腺轴 |
英文关键词: High temperature Hypertension Infarction Thyroid gland axis Adrenal cortex axis |
基金项目:北京市自然科学基金项目资助(NO.7072038) |
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中文摘要: |
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。 |
英文摘要: |
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(P<0.05). The ACTH and T4 decreased significantly(P<0.01), the TSH increased(P<0.05), 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. |
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