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目的：研究气温骤升导致高血压大鼠发生脑梗塞过程中单胺类神经递质的变化。方法：采用易卒中型肾血管性高血压 (RHRSP)模型，放置于人工模拟的气温骤升环境中诱发脑卒中，检测气温骤升前后大鼠单胺类神经递质E、NE 和DA 的变化。结果：气温骤升时，正常生理组大鼠血中NE 水平明显降低（P＜0.01），E 和DA 变化不明显；而当升温结束后，NE 出现明显的回升（P＜0.01），恢复到升温前水平，DA 继续下降，明显低于同组降温前和降温中水平（P＜0.01）。高血压大鼠血中的单胺类神经递质在气温骤升的刺激下出现异常升高，E、NE 和DA 浓度均比升温前明显的升高（P＜0.01），其中E 和NE 水平还明显地高于同一时间点的生理组大鼠（P＜0.01）。模型组升温后发生脑梗塞的大鼠血E 水平仍明显高于同一时间点的生理组大鼠（P＜0.05）和同组升温前水平（P＜0.01）。结论：在气温骤升的应激刺激下，高血压机体内单胺类神经递质的异常升高及其调节的紊乱是骤然高温诱发脑梗塞发病的重要机制。

英文摘要:

Objective: To investigate the effect of sudden rising temperature on the monoamine neurotransmitter in hypertensive rats with infarction. Methods: The improved rats model of strokes prone renovascular hypertensive (RHRSP) was used in this study, then they were carried out in man-made sudden high temperature to induce infarction. The changes of E, NE and DA before and after the temperature rise were detected. Results: Sudden rising temperature decreased the NE in the rats of normal group significantly （P＜0.01）, but did dose not change the E and DA. After rising temperature of normal groups, the level of NE increased significantly （P＜0.01）, but the level of DA dropped significantly （P＜0.01）. In the model groups, sudden rising temperature increased the levels of E,NE and DA significantly （P＜0.01）, the levels of E and NE were also higher than that of normal group at the same time （P＜0.01）. Moreover, the level of E in the rats with infarction after rising temperature was higher than that of normal group at the same time （P＜0.05）and the model group before rising temperature （P＜0.01）. Conclusion: The important mechanisms of infarction induced by sudden rising temperature are the abnormal increasing of monoamine neurotransmitter in the hypertension body and the disorder of adjusting it.

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