【摘要】 目的建立乐果诱导的迟发性神经病的大鼠模型,并观察其神经病理改变。方法随机将SD大鼠分成3组:高剂量组腹腔注射乐果乳油剂量为330mg/kg;低剂量组注射剂量为165mg/kg;对照组注射同量玉米油。观察染毒后急性中毒症状及中毒后活动、饮食等一般状况的变化;检测血清乙酰胆碱酯酶(AChE)活性变化;光镜和电镜观察周围神经的病理变化。结果实验第2周,高剂量组大鼠出现了轻微的步态不平衡;第4周时高剂量组大鼠出现了后肢肌力弱,有的后肢完全瘫痪。低剂量组在中毒后也出现了同样的症状。染毒组大鼠胫神经轴索内线粒体聚集,还可见到神经微丝排列紊乱。髓鞘普遍疏松,板层分离多见,板层间空泡化、气球样变,有的呈典型的葱管样改变,可见部分髓鞘缺失。结论用大鼠建立乐果迟发性神经病的动物模型是可行的。更多还原

【Abstract】 Objective To establish the rats OPIDP model induced by dimethoate and then to provide important academic evidence to the early diagnose and prevention of disease.Methods Healthy SD rats were divided into 3 groups randomly.Dimethoate were administered by ip at signal dosage of 165 and 330 mg/kg,and the control group was given some volum of corn oil.Results In high dose group,at 2 weeks after the initial exposure,the onset of OPIDN associated cilinical signs and syndrome occurs such as the muscle power of lower limb crura was decreased,the space between feet increased when rats laid on ground,the reaction of juxtaposition was slow after puncturing with acicula.At 4 weeks all above signs and syndrome were heavy.The same symptoms were also seen in the low dose group after exposure but they were light.In axon of nerve tibialis mitochondrion,neuro-microfilament and neuromicrotubule dereased.The myelin loosen generally,the separate of ply was popular,the vacuole was between plies,the change as balloon,some was the typical change as shallot.We could see some demyelination.Conclusion To establish the rats OPIDP model induced by dimethoate is available.更多还原