Fullerton P M, Barnes J M
Br J Ind Med. 1966 Jul;23(3):210-21. doi: 10.1136/oem.23.3.210.
Acrylamide produces ataxia and limb weakness in rats when given in repeated oral doses of 25 100 mg./kg. at various intervals or mixed with the diet in concentrations of 100 to 400 p.p.m. An electrophysiological and histological study of peripheral nerves has been carried out in chronical poisoned rats. In animals with severe clinical abnormalities, motor nerve conduction velocity in the fibr supplying the small muscles of the hind paw was reduced to approximately 80% of the control value. Histologically, degeneration of axis cylinders and myelin sheaths was found in peripheral nerve affecting predominantly the distal parts of the longest fibres. When paralysed animals were no longer given acrylamide, they recovered clinically, conduction velocity returned to the normal range, and there was histological evidence of regeneration of nerve fibres.
当以25至100毫克/千克的重复口服剂量，在不同间隔时间给予大鼠，或以100至400 ppm的浓度混入饮食中时，丙烯酰胺会使大鼠出现共济失调和肢体无力。已对慢性中毒大鼠的外周神经进行了电生理和组织学研究。在有严重临床异常的动物中，供应后爪小肌肉的纤维中的运动神经传导速度降低至对照值的约80%。组织学上，在外周神经中发现轴突和髓鞘变性，主要影响最长纤维的远端部分。当不再给瘫痪动物丙烯酰胺时，它们临床恢复，传导速度恢复到正常范围，并且有神经纤维再生的组织学证据。
