Burres S A, Richman D P, Crayton J W, Arnason B G
Muscle Nerve. 1979 May-Jun;2(3):186-90. doi: 10.1002/mus.880020306.
To study the basis for the myasthenic illness that develops in some patients receiving D-penicillamine (D-P), we measured neuromuscular transmission in D-P-treated guinea pigs. Treated animals manifested edrophonium chloride-repairable decremental responses to 30-Hz nerve stimulation (8.5% +/- 1.5%--mean +/- SEM; N = 16) compared with the response in saline-treated control animals (-0.3% +/- 0.85%, N = 10, p less than 0.005). Posttetanic phenomena were studied in 5 treated animals; 3 revealed posttetanic exhaustion. Miniature endplate potential (MEPP) amplitudes were significantly reduced in 11 treated animals (0.612 +/- 0.016 mV) compared with 6 controls (0.713 +/- 0.024 mV, p less than 0.01). The MEPP frequency appeared reduced in treated animals. Both MEPP amplitude and MEEP frequency correlated with the decrement.
为研究某些接受青霉胺(D-P)治疗的患者发生肌无力疾病的基础,我们检测了接受D-P治疗的豚鼠的神经肌肉传递情况。与接受生理盐水治疗的对照动物相比,接受治疗的动物对30赫兹神经刺激表现出依酚氯铵可修复的递减反应(8.5%±1.5%——平均值±标准误;N = 16),而对照动物的反应为(-0.3%±0.85%,N = 10,p<0.005)。对5只接受治疗的动物研究了强直后现象;3只出现强直后疲劳。与6只对照动物(0.713±0.024毫伏,p<0.01)相比,11只接受治疗的动物的微小终板电位(MEPP)幅度显著降低(0.612±0.016毫伏)。接受治疗的动物中MEPP频率似乎降低。MEPP幅度和MEEP频率均与递减反应相关。