家兔急性氨中毒时体感诱发电位的变化 |
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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 |
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作者姓名: | 李清君 李文斌 |
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作者单位: | 基础医学研究所病理生理学研究室 |
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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
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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 |
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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. |
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Keywords: | hepatic encephalopathy/metab ammonia/tox ammonia/blood evoked potentials somatosensory rabbits |
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