Hyperthermia combined with ethanol administration induces c-fos expression in the central amygdaloid nucleus of the mouse brain. A possible mechanism of heatstroke under the influence of ethanol intake

Hyperthermia combined with ethanol administration induces c-fos expression in the central amygdaloid nucleus of the mouse brain. A possible mechanism of heatstroke under the influence of ethanol intake
复制标题

DOI:
10.1007/s00414-008-0278-7
复制
发表时间:
2009-09-01
影响因子:
2.1
通讯作者:
Shojo, Hideki
Shojo, Hideki
中科院分区:
医学3区
文献类型:
--
作者:
Kibayashi, Kazuhiko;Nakao, Ken-ichiro;Shojo, Hideki

文献摘要

被引文献

相似文献

中暑被定义为核心体温上升超过40.6摄氏度,并伴有精神状态异常,如谵妄,惊厥或因暴露于环境高温而导致的昏迷。乙醇摄入是中暑的一个诱发因素,这是一个相当广泛的共识。本研究采用小鼠高温模型,在预先给予乙醇和不给予乙醇的情况下,鉴定中暑引起的脑变化。暴露于42摄氏度的高温,直到核心温度达到43摄氏度,然后暴露于37摄氏度15分钟,降低了血液中O(2)的分压水平。之前的乙醇管理和热暴露引起低血压,严重的代谢性酸中毒和呼吸衰竭,并因此,产生中暑。大脑的免疫组织化学显示,先前的乙醇管理增加了c-fos免疫反应神经元的数量,作为神经元激活的标志,在中央杏仁核,这是参与体温调节。这些结果表明,乙醇和热暴露的联合作用诱导中暑,这是与中央杏仁核的激活,暗示的病理生理和机制的影响下,乙醇摄入量中暑。
Heatstroke is defined as a core body temperature that rises above 40.6 degrees C and is accompanied by mental status abnormalities such as delirium, convulsions, or coma resulting from exposure to environmental heat. There is fairly wide agreement that ethanol intake is a predisposing factor in heatstroke. This study was performed to identify the brain changes induced by heatstroke, using a mouse hyperthermia model with and without preceding ethanol administration. Exposure to heat of 42 degrees C until the core temperature reached to 43 degrees C followed by exposure to 37 degrees C for 15 min decreased the levels of partial pressures of O(2) in blood. Preceding ethanol administration and heat exposure induced hypotension, severe metabolic acidosis and respiratory failure, and, accordingly, produced heatstroke. Immunohistochemistry of the brains showed that preceding ethanol administration increased the number of c-fos-immunoreactive neurons, as a marker of neuronal activation, in the central amygdaloid nucleus, which is involved in thermoregulation. These results indicate that combined effects of ethanol and heat exposure induce heatstroke that is associated with activation of the central amygdaloid nucleus, implicating the pathophysiology and mechanisms of heatstroke under the influence of ethanol intake.