Abstract

The mechanisms responsible for the incomplete recovery of muscle function after microneurovascular transfer have not been fully determined. Because fiber degeneration and regeneration can impact muscle mechanical function, the authors tested the null hypothesis that ischemia-induced fiber degeneration is not responsible for the force deficits observed after neurovascular muscle transfer. Rats were assigned to one of three groups: orthotopic, nonvascularized grafting of the extensor digitorum longus muscle (STD group); orthotopic, neurovascular transfer of the extensor digitorum longus muscle with no intraoperative ischemia (NV-0 group); or orthotopic, neurovascular transfer of the extensor digitorum longus muscle with 3 hours of intraoperative ischemia (NV-3 group). At 1 and 2 weeks, extensor digitorum longus muscle cross-sections were labeled for developmental myosin heavy chain isoforms, markers of fiber regeneration. In extensor digitorum longus muscles from animals in the STD group, many small cells strongly labeled for developmental myosin heavy chain were observed and identified as myoblasts, indicating recent muscle fiber necrosis with subsequent regeneration. Extensor digitorum longus muscles from rats in the NV-0 and NV-3 groups contained no cells labeled for developmental myosin heavy chain. After neurovascular muscle transfer (with ischemia times up to 3 hours), ischemia-induced muscle fiber degeneration and regeneration does not occur. Muscle fiber degeneration is not responsible for the force deficits observed after microneurovascular skeletal muscle transfer.

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