4-氨基吡啶和3,4-二氨基吡啶对兔实验性自身免疫重症肌无力的治疗

Therapy of experimental autoimmune myasthenia gravis in rabbits with 4-aminopyridine and 3,4-diaminopyridine

以N-AChR膜微囊免疫家兔,造成重症肌无力模型,iv 4-AP 0.8 mg·kg^(-1)后病兔的肌无力症状迅速缓解。以4Hz电流刺激坐骨神经,腓肠肌复合肌电位和足趾收缩即由递减变为整齐;50Hz电流引起的强直收缩能保持。作用维持9.1±2.5h。iv 3,4-DAP 0.4mg·kg^(-1)可获相似效果,持续9.3±3.1h。两药有明显的对症治疗作用。

The autoimmune myasthenia gravis (AMG) in rabbits was produced by in-tradermal injection of N-AChR-rich membrane vesicles isolated from the electric organ of Narcine limlei. After iv 4-aminopyridine (4-AP) 0. 8 mg·kg-1 to 8 AMG rabbits, their general posture improved promptly, the features of gastrocnemius compound action potentials and toe twitches elicited by 4-Hz stimuli applied to the sciatic nerve returned to normal , and the tetanic plateau evoked by 50-Hz indirect stimulation was again well sustained. This improved condition lasted 9. 1 ± 2. 5 h. Other 8 AMG rabbits given 3, 4-diaminopy-ridine (3,4-DAP) 0. 4 mg·kg-1 showed a similar improvement for 9. 3 ± 3. 1 h. These results indicated that 4-AP and 3,4-DAP were effective in treating the AMG in rabbits, they may be useful in the clinical treatment of myasthenia gravis patients.