Giusti, Guilherme

AbstractPurposeAnimal models can be helpful in evaluating new surgical strategies for brachial plexus reconstruction. While several groups have already used the rabbit brachial plexus to model injury, reports conflict in anatomic detail and do not identify a nerve‐muscle pair to measure motor function recovery after reconstruction. The purpose of the current study is to describe the innervations of the biceps and triceps muscles in rabbits, which are both amenable to study in brachial plexus injury models.Materials and MethodsThirteen rabbits weighing 2–2.5 kg were anesthetized. Six rabbits were sacrificed and dissected using loupe and microscope magnification to understand the overall morphology of the brachial plexus. Seven rabbits underwent electrophysiologic investigation. A bipolar nerve stimulator was used to systematically stimulate the roots, trunks and divisions, and nerve branches of the rabbit brachial plexus and compound muscle action potential was used to record muscle response. Nerve length and width measurements were not recorded.ResultsRoots contributing to the brachial plexus were C5, C6, C7, C8, and T1. In contrast to other anatomical studies, T2 did not contribute to the brachial plexus. The triceps was innervated by the radial nerve, which received contributions from C6 (1.6 mA), C7 (1.9 mA), C8, and T1 (12.2 mA).The biceps had dual innervation (proximally and distally). The proximal branch received contributions from C6 (3.5 mA) and C7 (5mA). The distal portion was innervated by a branch from the median nerve, which received innervation from C6, C7, C8, and T1.ConclusionsThe overall structure of rabbit brachial plexus is described and innervation of the biceps and triceps is described in detail. This anatomic investigation will form the basis of a future brachial plexus model of injury and repair.

Processed nerve allografts have become an alternative to repair segmental nerve defects, with results comparable with autografts regarding sensory recovery; however, they have failed to reproduce comparable motor recovery. The purpose of this study was to determine how revascularizaton of processed nerve allograft would affect motor recovery. Eighty‐eight rats were divided in four groups of 22 animals each. A unilateral 10‐mm sciatic nerve defect was repaired with allograft (group I), allograft wrapped with silicone conduit (group II), allograft augmented with vascular endothelial growth factor (group III), or autograft (group IV). Eight animals from each group were sacrificed at 3 days, and the remaining animals at 16 weeks. Revascularization was evaluated by measuring the graft capillary density at 3 days and 16 weeks. Measurements of ankle contracture, compound muscle action potential, tibialis anterior muscle weight and force, and nerve histomorphometry were performed at 16 weeks. All results were normalized to the contralateral side. The results of capillary density at 3 days were 0.99% ± 1.3% for group I, 0.33% ± 0.6% for group II, 0.05% ± 0.1% for group III, and 75.6% ± 45.7% for group IV. At 16 weeks, the results were 69.9% ± 22.4% for group I, 37.0% ± 16.6% for group II, 84.6% ± 46.6% for group III, and 108.3% ± 46.8% for group IV. The results of muscle force were 47.5% ± 14.4% for group I, 21.7% ± 13.5% for group II, 47.1% ± 7.9% for group III, and 54.4% ± 10.6% for group IV. The use of vascular endothelial growth factor in the fashion used in this study improved neither the nerve allograft short‐term revascularization nor the functional motor recovery after 16 weeks. Blocking allograft vascularization from surrounding tissues was detrimental for motor recovery. The processed nerve allografts used in this study showed similar functional motor recovery compared with that of the autograft. © 2014 Wiley Periodicals, Inc. Microsurgery 36:134–143, 2016.