Forensic Neuropathology of Hyperthermia

中暑定义为核心体温高于40.6℃，并伴有精神状态异常，如因暴露在环境高温下而导致的精神错乱、抽搐或昏迷。相当广泛的共识是，酒精摄入是中暑的一个诱因。这项研究是为了确定中暑引起的大脑变化，使用有无预先给予乙醇的小鼠体温过高模型。热暴露40℃直到核心温度达到42℃，再暴露37℃15min，可引起小鼠代谢性酸中毒和呼吸性碱中毒。免疫组织化学显示，高温小鼠大脑中央杏仁核(CEA)内参与体温调节的c-fos免疫反应神经元数量增加。预先给予乙醇使小鼠在热暴露后维持较高的核心温度，诱发低血压、严重代谢性酸中毒和呼吸衰竭，从而导致中暑，并进一步增加小鼠CEA内c-fos免疫反应神经元的数量。这些结果表明，体温升高与CEA中神经元的激活有关，乙醇的存在会加剧体温过高，这可能是中暑病因中脑功能障碍的病理生理学和机制之一。

Heatstroke is defined as a core body temperature that rises above 40.6 ℃ 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 40 ℃ until the core temperature reached to 42 ℃ followed by exposure to 37 ℃ for 15 min induced metabolic acidosis and respiratory alkalosis in mice. Immunohistochemistry of the brains of hyperthermia mice showed an increase in the number of c-fos immunoreactive neurons, as a marker of neuronal activation, in the central amygdaloid nucleus (CeA), which is involved in thermoregulation. Preceding ethanol administration maintained a high core temperature after heat exposure, induced hypotension, severe metabolic acidosis and respiratory failure, and accordingly, produced heatstroke, and further increased the number of c-fos immunoreactive neurons in the CeA in mice. These results indicate that hyperthermia is associated with neuronal activation in the CeA and is exacerbated by the presence of ethanol, implicating the pathophysiology and mechanisms of brain dysfunctions in the etiology of heatstroke.