Sanders D B, Johns T R, Eldefrawi M E, Cobb E E
Arch Neurol. 1977 Feb;34(2):75-9. doi: 10.1001/archneur.1977.00500140029004.
In rats immunized with purified acetylcholine receptor protein (AChRP) from Torpedo electroplax, a defect of neuromuscular transmission physiologically identical to that seen in myasthenia gravis developed. The most sensitive index of the neuromuscular blockage was miniature end-plate potential (MEPP) amplitude. As early as 24 hours after inoculation with AChRP, the thymus showed reactive changes that are probably nonspecific. Removal of the thymus before or within three days after immunization delayed, but did not prevent, development of reduced MEPP amplitude. Prednisolone given within 35 days after immunization produced reversal of MEPP reduction within 24 hours, but had no such immediate effect when given 15 days later. It is probable that prednisolone acted by reducing the immunologic responsiveness of the animals during the developing phase of the defect of neuromuscular transmission.
用从电鳐电器官纯化的乙酰胆碱受体蛋白(AChRP)免疫大鼠后,出现了一种神经肌肉传递缺陷,其生理表现与重症肌无力所见相同。神经肌肉阻滞最敏感的指标是微小终板电位(MEPP)幅度。早在接种AChRP后24小时,胸腺就出现了可能是非特异性的反应性变化。在免疫前或免疫后三天内摘除胸腺,虽延迟但并未阻止MEPP幅度降低的发展。免疫后35天内给予泼尼松龙,可在24小时内使MEPP降低得到逆转,但在15天后给予则没有这种即时效果。泼尼松龙可能是在神经肌肉传递缺陷的发展阶段通过降低动物的免疫反应性而起作用的。