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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 study the neuroendocrine mechanism of cerebral infarction in hypertensive rats caused by the sudden warming of temperature. Methods: The model of stroke-prone renovascular hypertension (RHRSP) was used to induce cerebral infarction in high-temperature environment where the simulated temperature suddenly increased. The changes of ACTH, CORT, TSH, T3 and T4 in rats before and after high-temperature stimulation were detected. Results: Sudden increase of temperature caused the ACTH and CORT in physiological rats increased. The levels of CORT, TSH, T3, T4 in model group were all increased while the level of ACTH was decreased (P <0.05). The levels of ACTH and T4 in cerebral infarction rats after warm-up were significantly lower than those before warm-up (P <0.01), while the levels of TSH were significantly higher than those before warm-up (P <0.05). CONCLUSIONS: Hypertension is characterized by disturbances in the stress response system, abnormal fluctuations of thyroid stimulating hormone and adrenocorticotropic hormone, and is an important neuroendocrine mechanism for the sudden onset of cerebral infarction in hypertensive patients with hypertension.