Lin M T, Kao T Y, Chio C C, Jin Y T
Department of Physiology, National Cheng Kung University Medical College, Tainan City, Taiwan, Republic of China.
Am J Physiol. 1995 Aug;269(2 Pt 2):H487-90. doi: 10.1152/ajpheart.1995.269.2.H487.
To explore the importance of brain dopamine in the heatstroke-induced striatal ischemia and neuronal injury, we compared the temporal profile of the heatstroke-induced striatal extracellular dopamine release, striatal blood flow, and striatal neuronal loss in rats with or without striatal dopamine depletion produced by 6-hydroxydopamine. In vivo voltammetry was used in rats to measure changes in extracellular concentrations of dopamine in the corpus striatum. Striatal neuronal damage was rated on a scale from zero to three (0, no damage; 3, maximum cell loss). The autoradiographic diffusible tracer technique was used for the measurement of striatal blood flow. After the onset of heatstroke, the heatstroke rats without brain dopamine depletion displayed hyperthermia, decreased mean arterial pressure, increased intracranial pressure, decreased cerebral perfusion pressure, decreased striatal blood flow, increased striatal dopamine release, and increased score of striatal neuronal damage as compared with those of normothermic controls. However, when the striatal dopamine system was destroyed by 6-hydroxydopamine, the heatstroke-induced arterial hypotension, intracranial hypertension, ischemic damage to the striatum, and elevated striatal dopamine release were reduced. In addition, the survival time of the heatstroke rats was prolonged after depleting striatal dopamine. Thus it appears that dopamine depletion protects striatal neurons from heatstroke-induced ischemia and cell death.
为了探究脑多巴胺在中暑诱导的纹状体缺血和神经元损伤中的重要性，我们比较了中暑诱导的纹状体细胞外多巴胺释放、纹状体血流量以及纹状体神经元损失在有或无由6-羟基多巴胺导致的纹状体多巴胺耗竭的大鼠中的时间变化情况。采用体内伏安法测量大鼠纹状体中细胞外多巴胺浓度的变化。纹状体神经元损伤按0至3级进行评分（0级，无损伤；3级，最大细胞损失）。使用放射自显影可扩散示踪技术测量纹状体血流量。中暑发作后，与正常体温对照组相比，未发生脑多巴胺耗竭的中暑大鼠表现出体温过高、平均动脉压降低、颅内压升高、脑灌注压降低、纹状体血流量减少、纹状体多巴胺释放增加以及纹状体神经元损伤评分增加。然而，当纹状体多巴胺系统被6-羟基多巴胺破坏后，中暑诱导的动脉低血压、颅内高压、纹状体缺血损伤以及纹状体多巴胺释放增加均有所减轻。此外，在耗尽纹状体多巴胺后，中暑大鼠的存活时间延长。因此，多巴胺耗竭似乎可保护纹状体神经元免受中暑诱导的缺血和细胞死亡。
