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家兔急性氨中毒时体感诱发电位的变化
引用本文:李清君 李文斌. 家兔急性氨中毒时体感诱发电位的变化[J]. 河北医科大学学报, 1998, 19(4): 193-196
作者姓名:李清君 李文斌
作者单位:基础医学研究所病理生理学研究室
摘    要:目的:探讨高血氨对神经传导及兴奋功能的影响。方法:观察家兔腔注入复方氯化铵溶流后,体感诱发电位(SEP)和外周感觉神经传导速度(SCV)的变化。结果:注入复方氯化争溶液后,SEP各成分峰潜伏期均延长,以P12和N15延长最明显,峰间潜伏期N9-P12和P12-N15亦延长,严重高氨血症时,P12和P15的振幅减小,但SCV无显著改变,结论:急性氨中毒可使中枢内神经传导发生延缓和神经元的兴功能出现异

关 键 词:氨中毒 急性 体感诱发电位 肝性脑病

CHANGES OF SOMATOSENSORY EVOKED POTENTIAL DURING ACUTE AMMONIA INTOXICATION IN RABBITS
Abstract:Objective: The present study was performed to explore the effect of hyperammonemia on neural conductivity and neuronal excitability in the somatosensory system. Methods: After intra intestinal administration of compound NH 4Cl solution, changes of somatosensory evoked potential(SEP) and sensory nerve conductive velocity(SCV) were observed in rabbits. Results:SEP changes after the administration were characterized by prolongation of latencies of all components, especially the cerebral components of P12 and N15, and by prolongation of inter-peak latencies of N9 P12 and P12 N15. The amplitudes of P12 and N15 were decreased in severe hyperammonemia, but SCV was not changed.Conclusion: Conductivity and excitability of the central part of the somatosensory pathway were involved in hyperammonemia,and the disfunction in the cerebral cortex was more serious than that of the subcortex structures.
Keywords:hepatic encephalopathy/metab  ammonia/tox  ammonia/blood  evoked potentials  somatosensory  rabbits
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