Kao T Y, Chio C C, Lin M T
Department of Physiology, National Cheng Kung University Medical College, Tainan City, Taiwan, ROC.
Stroke. 1994 Dec;25(12):2483-6; discussion 2486-7. doi: 10.1161/01.str.25.12.2483.
Brain dopamine has been implicated as a mediator of brain neuronal damage resulting from ischemic injury. Augmented interleukin-1 production and cerebral ischemia occurred during onset of heatstroke. This study has attempted to ascertain whether heatstroke resulting from hyperthermia causes an increase in hypothalamic dopamine release and to assess whether the administration of an interleukin-1 receptor antagonist (IL-1ra) can attenuate heat-stroke formation.
Both local cerebral blood flow and hypothalamic dopamine release during onset of heatstroke were assessed in saline-treated rats and in rats treated with an IL-1ra. Heat-stroke was induced by exposing the animals to a high ambient temperature. Hypothalamic dopamine release was determined by carbon fiber electrodes combined with in vivo differential pulse amperometry.
During onset of heatstroke, rats with heatstroke displayed higher values of colonic temperature, higher values of hypothalamic dopamine release, and lower values of blood flow in different brain regions compared with normothermic control rats. In another separate experiment in which IL-1ra (200 micrograms/kg IV) was injected 30 minutes before onset of heatstroke, both the augmented hypothalamic dopamine release and diminished cerebral blood flow during onset of heatstroke were significantly attenuated. In addition, the survival time (interval between onset of heatstroke and death) of the rats with heatstroke was prolonged by pretreatment with IL-1ra.
These results suggest that an increase in hypothalamic dopamine release and a decrease in local cerebral blood flow occur during onset of heatstroke. Pretreatment with IL-1ra attenuates the heatstroke formation resulting from cerebral ischemia by reducing hypothalamic dopamine release.
脑多巴胺被认为是缺血性损伤所致脑神经元损伤的介质。中暑发作时白细胞介素-1产生增加且发生脑缺血。本研究试图确定热射病是否会导致下丘脑多巴胺释放增加，并评估给予白细胞介素-1受体拮抗剂（IL-1ra）是否能减轻热射病的形成。
在生理盐水处理的大鼠和用IL-1ra处理的大鼠中，评估热射病发作期间的局部脑血流量和下丘脑多巴胺释放。通过将动物暴露于高环境温度来诱导热射病。采用碳纤维电极结合体内差分脉冲伏安法测定下丘脑多巴胺释放。
与体温正常的对照大鼠相比，热射病大鼠在热射病发作期间结肠温度更高、下丘脑多巴胺释放值更高，且不同脑区的血流量更低。在另一项单独实验中，在热射病发作前30分钟静脉注射IL-1ra（200微克/千克），热射病发作期间下丘脑多巴胺释放增加和脑血流量减少均得到显著减轻。此外，用IL-1ra预处理可延长热射病大鼠的存活时间（热射病发作至死亡的间隔时间）。
这些结果表明，热射病发作期间下丘脑多巴胺释放增加且局部脑血流量减少。用IL-1ra预处理可通过减少下丘脑多巴胺释放来减轻脑缺血所致的热射病形成。
