Heatstroke-induced cerebral ischemia and neuronal damage - Involvement of cytokines and monoamines
Heatstroke-induced cerebral ischemia and neuronal damage - Involvement of cytokines and monoamines
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DOI：
10.1111/j.1749-6632.1997.tb51748.x
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发表时间：
1997-01-01
期刊：
影响因子：
--
通讯作者：
Lin, MT
中科院分区：
文献类型：
--
作者：
Lin, MT
为确定脑单胺类物质和细胞因子水平是否参与中暑所致的脑缺血和神经元损伤，进行了实验。将麻醉大鼠暴露在42摄氏度的高温环境中，诱发中暑；平均动脉压从峰值水平开始下降的时刻被视为中暑的开始。结果发现，在中暑引起的脑缺血和神经元损伤过程中，下丘脑、纹状体和其他脑区的多巴胺、5-羟色胺和去甲肾上腺素的胞外浓度升高。此外，中暑后大鼠血浆和脑组织中IL-1、IL-6和肿瘤坏死因子的浓度也明显升高。脑内注射6-羟基多巴胺或5，7-二羟色胺产生的多巴胺或5-羟色胺分别可减少中暑所致的脑缺血和神经元损伤。因此，在脑多巴胺或5-羟色胺耗尽后，这些中暑大鼠的存活率增加。此外，用IL-1受体拮抗剂阻断IL-1受体可减轻中暑所致的脑缺血、神经元损伤和单胺蓄积。热休克蛋白诱导后，中暑大鼠的存活率也有所提高。结果提示，脑内多巴胺、5-羟色胺和IL-1的显著蓄积是中暑大鼠脑缺血和神经元损伤的重要原因。通过抑制脑内IL-1受体或单胺系统，以及通过诱导热休克蛋白，可提高中暑大鼠的存活率。
Experiments were carried out to ascertain whether the levels of brain monoamines and cytokines are involved in the heatstroke-induced cerebral ischemia and neuronal damage. Heatstroke was induced by exposing anesthetized rats to a high ambient temperature of 42 degrees C; the moment at which the mean arterial pressure began to decrease from its peak level was taken as the onset of heatstroke. It was found that, during the heatstroke-induced cerebral ischemia and neuronal damage, the extracellular concentration of either dopamine, serotonin or norepinephrine were increased in the hypothalamus, the corpus striatum and other brain regions. In addition, the concentration of interleukin-1 (IL-1), IL-6 and tumor necrosis factor in both the plasma and brain was also increased during heatstroke-induced cerebral ischemia and neuronal damage. Heatstroke-induced cerebral ischemia and neuronal damage were attenuated by depletion of brain dopamine or serotonin produced by intracerebral injection of 6-hydroxydopamine or 5, 7-dihydroxytryptamine, respectively. Accordingly, the survival of these heatstroke rats was increased after brain dopamine or serotonin depletion. Furthermore, heatstroke-induced cerebral ischemia, neuronal damage and monoamine accumulation were attenuated by blockade of IL-1 receptor produced by treatment with an IL-1 receptor antagonist. The survival of the heatstroke rats was also increased after induction of heat shock protein. The results suggest that marked accumulation of either dopamine, serotonin or IL-1 in brain is important for the occurrence of heatstroke-induced cerebral ischemia and neuronal damage in rats. The survival of these heatstroke rats can be increased by inhibition of IL-1 receptors or monoamine system in brain as well as by induction of heat shock protein.