BACKGROUND: Abdominal wall vascularized composite allotransplantation is the second most common form of vascularized composite allotransplantation. Sensory and functional recovery are expected in other forms but have never been demonstrated in abdominal wall vascularized composite allotransplantation. The authors hypothesize that coaptation of two thoracolumbar nerves will result in reinnervation of the alloflap and maintenance of the muscle component. METHODS: Adult, male, 10-week-old Brown Norway and Lewis rats were used for experiments. The rat donor's common iliac vessels were anastomosed to the recipient's femoral vessels. Intercostal nerves T10/L1 were coapted. Four groups (n = 5 per group) were included for study: group 1, Lewis, intercostal nerves cut, not repaired; group 2, Lewis intercostal nerves cut, T10/L1 repaired; group 3, allogeneic Brown Norway-to-Lewis abdominal wall vascularized composite allotransplantation, T10/L1 repaired; and group 4, syngeneic Lewis-to-Lewis abdominal wall vascularized composite allotransplantation, T10/L1 repaired. Animals were killed on postoperative day 60. Nerve regeneration was assessed using muscle weight analysis, myofibril cross-sectional area, nerve histomorphometry, and neuromuscular junction percentage reinnervation. RESULTS: Groups 2, 3, and 4 maintained a significantly greater percentage of postharvest weight compared with group 1 (p < 0.05). Group 1 had significantly decreased myofibril cross-sectional area compared with controls (p < 0.05). There was no significant difference in myofibril cross-sectional area in groups 2 through 4 compared with controls (p > 0.05). Group 1 had significantly decreased percentage reinnervation of the alloflap compared with controls (p < 0.05). There was no significant difference when comparing group 2 through 4 with internal, contralateral controls (p > 0.05). CONCLUSION: In a murine model for abdominal wall vascularized composite allotransplantation, coaptation of T10/L1 will allow for reinnervation of the alloflap and maintenance of the muscle component.
BACKGROUND: Abdominal wall vascularized composite allotransplantation is the second most common form of vascularized composite allotransplantation. Sensory and functional recovery are expected in other forms but have never been demonstrated in abdominal wall vascularized composite allotransplantation. The authors hypothesize that coaptation of two thoracolumbar nerves will result in reinnervation of the alloflap and maintenance of the muscle component. METHODS: Adult, male, 10-week-old Brown Norway and Lewis rats were used for experiments. The ratdonor's common iliac vessels were anastomosed to the recipient's femoral vessels. Intercostal nerves T10/L1 were coapted. Four groups (n = 5 per group) were included for study: group 1, Lewis, intercostal nerves cut, not repaired; group 2, Lewis intercostal nerves cut, T10/L1 repaired; group 3, allogeneic Brown Norway-to-Lewis abdominal wall vascularized composite allotransplantation, T10/L1 repaired; and group 4, syngeneic Lewis-to-Lewis abdominal wall vascularized composite allotransplantation, T10/L1 repaired. Animals were killed on postoperative day 60. Nerve regeneration was assessed using muscle weight analysis, myofibril cross-sectional area, nerve histomorphometry, and neuromuscular junction percentage reinnervation. RESULTS: Groups 2, 3, and 4 maintained a significantly greater percentage of postharvest weight compared with group 1 (p < 0.05). Group 1 had significantly decreased myofibril cross-sectional area compared with controls (p < 0.05). There was no significant difference in myofibril cross-sectional area in groups 2 through 4 compared with controls (p > 0.05). Group 1 had significantly decreased percentage reinnervation of the alloflap compared with controls (p < 0.05). There was no significant difference when comparing group 2 through 4 with internal, contralateral controls (p > 0.05). CONCLUSION: In a murine model for abdominal wall vascularized composite allotransplantation, coaptation of T10/L1 will allow for reinnervation of the alloflap and maintenance of the muscle component.