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急性一氧化碳(CO)中毒是一种常见的职业性和生活性中毒。关于CO的毒性作用及中毒机制国内外已有较多报道。但对其神经毒性机制,特别是迟发脑病的机制尚未被阐明。一般认为,急性中毒时,血中碳氧血红蛋(COHb)含量明显增高,抑制了输氧功能,由于脑缺氧而出现一系列中枢神经系统中毒症状。为了探索急性CO中毒对中枢神经功能的影响,应用大鼠急性CO中毒模型观察其视觉诱发电位和体感诱发电位的变化。
Acute carbon monoxide (CO) poisoning is a common occupational and life poisoning. On the toxic effects of CO and poisoning mechanisms have been more reports at home and abroad. However, the mechanisms of their neurotoxic mechanisms, especially delayed encephalopathy, have not yet been elucidated. Generally believed that acute poisoning, the blood carboxyhemoglobin (COHb) content was significantly increased, inhibiting oxygen function, due to cerebral hypoxia and a series of symptoms of central nervous system poisoning. In order to explore the impact of acute CO poisoning on central nervous system function, the changes of visual evoked potential and somatosensory evoked potential were observed in acute CO poisoning model in rats.