Delay of denervation atrophy by sensory protection in an end-to-side neurorrhaphy model: A pilot study

Object: Temporary sensory innervation delays the atrophy process. A major disadvantage of most experimental models is that sensory-protected muscles must be denervated a second time to allow reinnervation by the affected nerve. The aim of this study was to assess the effect of sensory protection on denervated gastrocnemius muscle in an end-to-side neurorrhaphy model, in which denervated muscles may be preserved until axons of the native nerve reach their target without the necessity for a second operation. Methods: The tibial nerve of 24 female Lewis rats was transected. Twelve animals acted as the controls. In the other 12 animals, the end of the sural nerve was connected to the side of the distal tibial nerve stump (sensory protection group). At 5 and 10 weeks, wet gastrocnemius muscle weight was reported as a ratio of the operated to the unoperated side. For histological analysis, muscle samples were rapidly frozen and sections were stained with haematoxylin and eosin, Oil Red O stain and modified Gomori trichrome stain. Results: The difference between the sensory protection group and the control group was statistically significant at 5 (0.36 +/- 0.01 and 0.29 +/- 0.01, respectively; p < 0.001) and 10 weeks postoperatively (0.28 +/- 0.01 and 0.19 +/- 0.00, respectively; p < 0.001). Histological observations revealed that sensory-protected muscles underwent less atrophy. Conclusion: Sensory protection delays atrophy in an end-to-side neurorrhaphy model. (C) 2010 British Association of Plastic, Reconstructive and Aesthetic Surgeons. Published by Elsevier Ltd. All rights reserved

Significant reduction in neural adhesions after administration of the regenerating agent OTR4120, a synthetic glycosaminoglycan mimetic, after peripheral nerve injury in rats

Object. Extradural and intraneural scar formation after peripheral nerve injury frequently causes tethering and compression of the nerve as well as inhibition of axonal regeneration. Regenerating agents (RGTAs) mimic stabilizing and protective properties of sulphated glycosaminoglycan toward heparin-binding growth factors. The aim of this study was to assess the effect of an RGTA known as OTR4120 on extraneural fibrosis and axonal regeneration after crush injury in a rat sciatic nerve model. Methods. Thirty-two female Wistar rats underwent a standardized crush injury of the sciatic nerve. The animals were randomly allocated to RGTA treatment or sham treatment in a blinded design. To score neural adhesions, the force required to break the adhesions between the nerve and its Surrounding tissue was measured 6 weeks after nerve crush injury. To assess axonal regeneration, magnetoneurographic measurements were performed after 5 weeks. Static footprint analysis was performed preoperatively and at Days 1, 7, 14, 17, 21, 24, 28, 35, and 42 postoperatively. Results. The magnetoneurographic data show no significant difference in conduction capacity between the RGTA and the control group. In addition, results of the static footprint analysis demonstrate no improved or accelerated recovery pattern. However, the mean pullout force of the RGTA group (67 +/- 9 g [mean +/- standard error of the mean.]) was significantly (p < 0.001) lower than that of the control group (207 +/- 14 g [mean +/- standard error of the mean]). Conclusions. The RGTAs strongly reduce nerve adherence to surrounding tissue after nerve crush injury. (DOI: 10.3171/JNS/2008/109/11/0967