延迟神经修复后的恢复：一种药物辅助剂在灵长类动物模型中的影响
Recovery after delayed nerve repair: influence of a pharmacologic adjunct in a primate model.
作者信息
Badalamente M A, Hurst L C, Stracher A
机构信息
Department of Orthopaedics, School of Medicine, State University of New York, Stony Brook 11794.
出版信息
J Reconstr Microsurg. 1992 Sep;8(5):391-7. doi: 10.1055/s-2007-1006724.
Inhibition of calpains in skeletal muscle by the tripeptide, leupeptin, after median-nerve transection in the mid-forearm and a delayed nerve repair of 3-weeks duration, was studied in a primate (Cebus apella) model. Results indicated that leupeptin facilitates axon regrowth and neuromuscular recovery after delayed nerve repair. Toxicologic testing showed that leupeptin, administered at 18 mg/kg intramuscularly, twice daily for 24 weeks after delayed nerve repair, did not adversely affect hematology, clotting, blood chemistry, or echocardiogram profiles. These data indicate that leupeptin is an effective and safe adjunct to delayed nerve repair.
在灵长类动物（僧帽猴）模型中，研究了在正中神经于前臂中部横断并进行为期3周的延迟神经修复后，三肽亮抑酶肽对骨骼肌中钙蛋白酶的抑制作用。结果表明，亮抑酶肽促进延迟神经修复后的轴突再生和神经肌肉恢复。毒理学测试表明，在延迟神经修复后，以18mg/kg的剂量每日两次肌肉注射亮抑酶肽，持续24周，对血液学、凝血、血液化学或超声心动图检查结果均无不良影响。这些数据表明，亮抑酶肽是延迟神经修复的一种有效且安全的辅助药物。
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