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目的研究气温骤降导致高血压大鼠发生脑出血的神经内分泌机制。方法采用易卒中型肾血管性高血压大鼠(RHRSP)模型。将生理组、模型组和假手术组大鼠放置于人工模拟气候箱中进行气温骤降的处理。气温骤降后通过脑组织的大体观察确定脑出血的发生,并用放射免疫法检测气温骤降前后各组大鼠促肾上腺皮质激素(ACTH)、皮质酮(CORT)、促甲状腺激素(TSH)、三碘甲状腺原氨酸(T3)、四碘甲状腺原氨酸(T4)的动态变化。结果降温前,模型组大鼠肾上腺皮质轴激素水平和甲状腺轴激素的水平均低于相应的生理组大鼠(P<0.05或P<0.01)。但当气温骤降时,生理组大鼠ACTH、CORT、TSH水平均较降温前明显下降(P<0.05或P<0.01),而模型组大鼠肾上腺皮质轴激素(ACTH)和甲状腺轴激素(TSH、T4)的水平均比降温前显著上升(P<0.05或P<0.01)。降温后,生理组大鼠ACTH和TSH水平有所提高,但CORT、T3和T4水平仍然维持降低的趋势,模型组大鼠血中ACTH、CORT、TSH的水平仍然维持高位,并明显高于降温前水平(P<0.05或P<0.01)。结论肾上腺皮质轴和甲状腺轴的异常应激反应性增强,是气温骤降促发高血压脑出血发病的重要机理之一。
Objective To study the neuroendocrine mechanism of cerebral hemorrhage in hypertensive rats induced by the sudden drop in temperature. Methods Stroke-prone renovascular hypertensive rats (RHRSP) model was used. Physiological group, model group and sham operation group rats were placed in simulated climate chamber for temperature drop treatment. The brain hemorrhage was determined by general observation of brain tissue after temperature plunged, and the levels of ACTH, CORT, TSH, Triiodothyronine (T3), tetraiodothyronine (T4) in the dynamic changes. Results Before cooling, the levels of corticotropin and thyroid hormone in model group were lower than those in the corresponding physiological groups (P <0.05 or P <0.01). However, the ACTH, CORT and TSH levels in the physiology group were significantly lower than those before the temperature drop (P <0.05 or P <0.01), while the ACTH and thyroid axis hormone TSH, T4) were significantly higher than those before cooling (P <0.05 or P <0.01). After cooling down, the levels of ACTH and TSH in physiological rats were increased, but the levels of CORT, T3 and T4 still maintained a decreasing trend. The levels of ACTH, CORT and TSH in the blood of rats in model group remained high, Pre-level (P <0.05 or P <0.01). Conclusion Abnormal adrenocortical axis and thyroid axis increased abnormal stress response, which is one of the important mechanisms of sudden onset of temperature-induced hypertensive intracerebral hemorrhage.