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首页> 外文期刊>Clinical and experimental pharmacology & physiology >Pathogenesis of an experimental heatstroke model.
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Pathogenesis of an experimental heatstroke model.

机译：实验性中暑模型的发病机制。

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1. Heatstroke was induced by exposure under general anaesthesia to a high ambient temperature. The moment in which the mean arterial pressure (MAP) began to decrease from its peak level was taken as the onset of heatstroke. 2. Compared with normothermic controls, rats with heatstroke had higher values for colon temperature, neuronal damage score and heart rate, but lower MAP and cerebral blood flow. 3. Induction of heat shock protein, antagonism of interleukin-1 or N-methyl-D-aspartate receptors or depletion of brain monoamines protects against the heatstroke-induced arterial hypotension and cerebral ischaemic injury. 4. Thus, it appears that arterial hypotension and cerebral ischaemic damage is the main reason for development of heatstroke syndromes.
机译：1.在全身麻醉下暴露于高环境温度下诱发中暑。平均动脉压（MAP）从峰值开始下降的时刻被视为中暑。 2.与正常体温对照组相比，中暑大鼠的结肠温度，神经元损伤评分和心率值较高，但MAP和脑血流量较低。 3.诱导热休克蛋白，拮抗白介素1或N-甲基-D-天冬氨酸受体或脑单胺耗竭，可防止中暑引起的动脉低血压和脑缺血。 4.因此，看来动脉低血压和脑缺血损伤是中暑综合征发展的主要原因。

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