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目的 探讨高原缺氧条件下梭曼中毒大鼠脑组织乙酰胆碱酯酶 (AChE)活性和毒蕈碱样乙酰胆碱 (M)受体变化规律。方法 以DTNB法和受体放射性配基结合法检测大鼠皮层、海马及纹状体AChE活性和M受体密度及亲和力。结果 缺氧使大鼠脑组织AChE活性不同程度升高 ,缺氧 2 4h海马和纹状体M受体密度分别增加 10 .4%和 2 5 .3 % ,M受体的亲和力分别增加 5 5 .6 %和 30 .3 %。单纯梭曼中毒和缺氧复合梭曼中毒均显著抑制脑组织AChE活性 ,但缺氧条件下梭曼对大鼠海马和纹状体的AChE抑制程度减弱。缺氧和缺氧复合梭曼中毒脑损伤以纹状体最明显。结论 高原缺氧和梭曼中毒均明显干扰大鼠脑组织胆碱能神经系统功能。
Objective To investigate the changes of acetylcholinesterase (AChE) activity and muscarinic acetylcholine (M) receptors in brain tissue of soman-poisoned rats under high altitude hypoxia. Methods The AChE activity and M receptor density and affinity of rat cortex, hippocampus and striatum were detected by DTNB method and receptor radioligand binding assay. Results Hypoxia increased the activity of AChE in rat brain tissue to different extents. The density of M receptor in hippocampus and striatum increased by 10.4% and 25.3%, respectively, and the affinity of M receptor increased by 5 5 .6% and 30.3%. Both soman and hypoxia combined soman poisoning significantly inhibited AChE activity in brain tissue. However, the inhibition of AChE by soman in rat hippocampus and striatum under hypoxia was weakened. Hypoxia and hypoxia recombination soman intoxication brain damage striatum most obvious. Conclusion Both plateau hypoxia and soman poisoning obviously interfere the cholinergic nervous system function of rat brain.