Chen S M
Department of Pharmacology, Chinese PLA General Hospital, Beijing.
Zhonghua Shen Jing Jing Shen Ke Za Zhi. 1991 Jun;24(3):169-73, 189.
All of 39 rabbits immunized with acetylcholine receptors invariably formed anti-AChR Abs and some of them developed muscular weakness or flaccid paralysis. Pharmacological, physiological and ultrastructural studies indicated that the pathology of experimental autoimmune myasthenia gravis in rabbits resembled that of human myasthenia gravis. The titer of anti-AChR Abs correlated poorly with disease severity and did not simply predicted the muscular weakness. The results ruled out the possibility that antigenic modulation of AChR was sufficient to account for the induction of myasthenia gravis. There was a close relationship between the sensitivity to curare and disease severity, but only part of immunized animals appeared electromyogram change. This led us to conclude that serum anti-AChR concentration would not be the single pathological factor in myasthenia gravis and disease severity may correlate with amount of normal AChR.
用乙酰胆碱受体免疫的39只兔子均产生了抗AChR抗体,其中一些出现了肌无力或弛缓性麻痹。药理学、生理学和超微结构研究表明,兔实验性自身免疫性重症肌无力的病理与人类重症肌无力相似。抗AChR抗体滴度与疾病严重程度相关性较差,不能简单地预测肌无力。结果排除了AChR抗原调节足以解释重症肌无力诱导的可能性。对箭毒的敏感性与疾病严重程度密切相关,但只有部分免疫动物出现肌电图改变。这使我们得出结论,血清抗AChR浓度不是重症肌无力的唯一病理因素,疾病严重程度可能与正常AChR的数量相关。