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缺氧诱导的低温通过去甲肾上腺素和一氧化氮在视前区腹内侧区介导。

Hypoxia-induced hypothermia mediated by noradrenaline and nitric oxide in the rostromedial preoptic area.

机构信息

Health Promotion and Exercise Program, National Institute of Health and Nutrition, 1-23-1 Toyama, Shinjuku 162-8636, Japan.

出版信息

Neuroscience. 2011 Apr 14;179:170-8. doi: 10.1016/j.neuroscience.2011.01.056. Epub 2011 Jan 28.

DOI:10.1016/j.neuroscience.2011.01.056
PMID:21277355
Abstract

Central nitric oxide (NO) has an important role in hypothermia induced by hypoxia as well as in that elicited by noradrenaline (NA) microinjected into the rostromedial preoptic area (POA) of the hypothalamus. Here, I tested the hypothesis that activation of adrenoceptors and NO in the rostromedial POA is involved in hypoxia-induced hypothermia in urethane-chloralose-anesthetized, neuromuscularly blocked, artificially ventilated rats. Hypoxic ventilation (10% O2-90% N2, 5 min) evoked an increase in the tail skin temperature and a decrease in the colonic temperature, though these changes occurred at 30 s to 7 min after returning the rats to ventilation with room air. These responses were eliminated by prior bilateral transection of the carotid sinus nerves, but not by bilateral cervical vagotomy, suggesting the involvement of activated carotid chemoreceptors in the hypoxic ventilation-induced hypothermia. Such responses were also greatly attenuated by the microinjection of an NO synthase (NOS) inhibitor, NG-monomethyl-L-arginine (L-NMMA, 25 nmol), but not by that of its inactive enantiomer, NG-monomethyl-D-arginine (D-NMMA, 25 nmol), into the NA-sensitive, hypothermia-inducing site in the rostromedial POA. Pretreatment with the α1-adrenoceptor blocker prazosin (50 pmol), but not vehicle saline, also greatly attenuated the hypoxic ventilation-induced heat loss responses. These results suggest that this hypoxia-induced hypothermia was mediated, at least in part, by activation of α1-adrenoceptors and NOS in the rostromedial POA.

摘要

中枢一氧化氮(NO)在缺氧诱导的低温和去甲肾上腺素(NA)注射到下丘脑的穹隆前区(POA)引起的低温中起重要作用。在这里,我测试了这样一个假设,即在罗慕达尔前区(POA)中的肾上腺素能受体和 NO 的激活参与了缺氧诱导的氯醛-尿烷麻醉、神经肌肉阻断、人工通气大鼠的低温。缺氧通气(10% O2-90% N2,5 分钟)引起尾巴皮肤温度升高和结肠温度降低,尽管这些变化发生在大鼠返回室内空气通气后的 30 秒至 7 分钟。这些反应被双侧颈动脉窦神经切断术消除,但不是双侧颈迷走神经切断术,这表明激活的颈动脉化学感受器参与了缺氧通气引起的低温。这种反应也被微注射一氧化氮合酶(NOS)抑制剂 NG-单甲基-L-精氨酸(L-NMMA,25 nmol)大大减弱,但不是其非活性对映体 NG-单甲基-D-精氨酸(D-NMMA,25 nmol),进入 NA 敏感、引起低温的罗慕达尔前区。预先用 α1-肾上腺素能受体阻滞剂哌唑嗪(50 pmol)处理,而不是用载体盐水处理,也大大减弱了缺氧通气引起的热量损失反应。这些结果表明,这种缺氧诱导的低温至少部分是通过罗慕达尔前区(POA)中的 α1-肾上腺素能受体和 NOS 的激活介导的。

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