鸡甲胺磷中毒性神经肌病模型的建立及电生理研究  

The electrical physiological detection and model formation of methamidophos induced toxic neuromyopathy in hens

作　　者：胡轶虹[1] 金梅香[1] 郭尔平[1] 江新梅[2] 

机构地区：[1]吉林省人民医院神经内科,吉林长春130021 [2]吉林大学第一医院神经内科,吉林长春130021

出　　处：《中风与神经疾病杂志》2012年第8期719-721,共3页Journal of Apoplexy and Nervous Diseases

摘　　要：目的建立鸡甲胺磷中毒迟发性神经病模型;通过周围神经电生理检测确定周围神经损伤情况并做预后评估。方法莱亨母鸡随机分为5组,甲胺磷经消化道染毒,染毒后1、2、3、4、8w取鸡坐骨神经进行电生理检测。结果甲胺磷致迟发性神经病早期以轴索损害为主(波幅降低),继之出现脱髓鞘改变(远端潜伏期延长及运动神经传导速度减慢)。结论 (1)利用甲胺磷染毒莱亨鸡可成功构建迟发性神经病模型;(2)电生理检测阳性率高,且早于临床体征的出现,是诊断迟发性神经病的客观指标之一。Objective To form the model of delayed toxic neuromyopathy in hens induced by methamidophos and to detect the injury of periphery nerve after treatment with methamidophos and evaluate the prognosis.Methods Fifty Leghorn hens were divided into 5 groups at random（n=10）.Experimental groups were given methamidophos through a cannula by mouth and were injected atropine sulfate to live through urgent period.At the end of 1,2,3,4,8 week after poisoning,sciatic nerves were dissociated and carried out electricity physiological test.Results Methamidophos induced delayed neuropathy showed priority to axis damage in the first week（amplitude recede）,afterwards at the second week showed demyelination（terminal latent period prolong and motor nerve conduction velocity slower）.Till the eighth week,motor nerve conduction velocity and terminal latent period had renewed to normal.Conclusion The model of delayed toxic neuromyopathy can be built successfully in Leghorn hens induced by methamidophos.The changes of electrical physiology happened earlier than that of clinical signs,yet it had a high positivity,so electrical physiological detect is a external index to diagnose OPIDN.

关 键 词：甲胺磷 迟发性神经病 周围神经电生理 

分 类 号：R745.7[医药卫生—神经病学与精神病学]