Recovery after delayed nerve repair: influence of a pharmacologic adjunct in a primate model.
Recovery after delayed nerve repair: influence of a pharmacologic adjunct in a primate model.
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延迟神经修复后的恢复：灵长类动物模型中药理学辅助剂的影响。
DOI：
10.1055/s-2007-1006724
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发表时间：
1992
影响因子：
2.1
通讯作者：
Stracher,A
中科院分区：
文献类型：
--
作者：
Badalamente,MA;Hurst,LC;Stracher,A
在灵长类动物（Cebus apella）模型中，研究了在前臂中段正中神经切断和延迟神经修复3周后，三肽亮抑酶肽对骨骼肌中钙蛋白酶的抑制作用。结果表明，亮抑酶肽促进轴突再生和延迟神经修复后的神经肌肉恢复。毒理学试验表明，在延迟神经修复后，肌内给予亮抑酶肽18 mg/kg，每日两次，持续24周，对血液学、凝血、血液化学或超声心动图特征无不良影响。这些数据表明亮抑酶肽是一种有效和安全的辅助延迟神经修复。
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.