Fetal nerve grafts preserved at deep breezing were used to repair the peripheral nerve defects. The nerve directs included the sural nerves (removed as the donor nerve in repairing other nerve defects) in 5 cases, and digital nerve in 2 cases. All of them got good sensitive function. Patients were followed up for 1 yeas, all patients had gained comparatively good sensation. The surgical technique was introduced, and the validity of the transplantation of fetal nerve was discussed.
To observe the effect of allogenic transplantation of deep frozen nerve in repairing sensory nerve defect, 22 patients who had received this type of treatment were followed up for 0.5-5 years. There were 18 males and 4 females in this group, and the average age was 28 years old. Thirty-six nerve defects including the common volar digital nerve, proper volar digital nerve were repaired by allograft of nerves stored at deep frozen (-80 degrees C). The storation period was ranged from 9 days to 1 years. The length of the nerves were 2 cm-12 cm. After follow-up for 3 years (ranged from 7 months-5 years), 23 cases of nerve allograft obtained excellent and good results (63.9%), 10 cases were fair (27.7%) and 3 cases were poor (8.3%). It was concluded that (1) frozen nerve is one of nice materials for repairing the nerve defect (lt; 5 cm); (2) the immunity of allogenenic nerve is weak; (3) the deep frozen storation can reduce the immunity of nerve; (4) the dimethyl sulfoxide can prevent the nerve tissue from injury by deep frozen; (5) the best temperature and period for deep frozen storation should be studied further.
Basing on the experimental results, 48 nerve defects (with the length of 3-4 cm in 21 cases, 4.1-5cm in 25 cases and 6cm in 2 cases) were repaired clinically by using vaseularized nerve sheath canal with living Schwann s cells, 87.5 percent of them obtained good results. The advantages were: (1) The neural sheath had rich blood supply with resultant less scar from its healing; (2) The living Schwann s cells would secrete somatomedin to promote the reproduction of neural tissues; and (3) The useless neurofib...
To find new technique for repair of peripheral nerve defect, the nerve elongation repair technique was adopted. Two cases with nerve defect were treated by this method. One was a 12 year old male, the defect length of right radial nerve was 7.2 cm at the elbow. The other one was a 28 year old male, the defect length of left ulnar nerve the was 5 cm at elbow. In this method, the nerve was elongated by slow stretch from distal and proximal end of the ruptured nerve. After a few days, the nerve was repaired by direct suture. After operation, the function of nerves were recovered in 119 days and 114 days respectively. Follow-up for 5 years, the function of the effected limbs were recovered to the normal side. It was concluded that: (1) the peripheral never can be elongated by slow stretch; (2) to stretch the nerve end in a rubber tube can prevent adhesion and connective tissue blocking; (3) strength and supporting point of stretching should be designed carefully.
ObjectiveTo summarize the research progress of autologous vein nerve conduit for the repair of peripheral nerve defect. MethodsThe recent domestic and foreign literature concerning autologous vein nerve conduit for repair of peripheral nerve defect was analyzed and summarized. ResultsA large number of basic researches and clinical applications show that the effect of autologous venous nerve conduit is close to that of autologous nerve transplantation in repairing short nerve defect, especially the compound nerve conduit has a variety of autologous nerve tissue, cells, and growth factors, etc. ConclusionAutologous vein nerve conduit for repair of non-nerve defect can be a good supplement of autologous nerve graft, improvement of autologous venous catheter to repair peripheral nerve defect is the research direction in the future.
OBJECTIVE: To explore the possibility to bridge peripheral nerve defects by xenogeneic acellular nerve basal lamina scaffolds. METHODS: Thirty SD rats were randomly divided into 5 groups; in each group, the left sciatic nerves were bridged respectively by predegenerated or fresh xenogeneic acellular nerve basal lamina scaffolds, autogenous nerve grafting, fresh xenogeneic nerve grafting or without bridging. Two kinds of acellular nerve basal lamina scaffolds, extracted by 3% Triton X-100 and 4% deoxycholate sodium from either fresh rabbit tibial nerves or predegenerated ones for 2 weeks, were transplanted to bridge 15 mm rat sciatic nerve gaps. Six months after the grafting, the recovery of function was evaluated by gait analysis, pinch test, morphological and morphometric analysis. RESULTS: The sciatic nerve function indexes (SFI) were -30.7% +/- 6.8% in rats treated with xenogeneic acellular nerve, -36.2% +/- 9.7% with xenogeneic predegenerated acellular nerve, and -33.9% +/- 11.3% with autograft respectively (P gt; 0.05). The number of regenerative myelinated axons, diameter of myelinated fibers and thickness of myelin sheath in acellular xenograft were satisfactory when compared with that in autograft. Regenerated microfascicles distributed in the center of degenerated and acellular nerve group. The regenerated nerve fibers had normal morphological and structural characters under transmission electron microscope. The number and diameter of myelinated fibers in degenerated accellular nerve group was similar to that of autograft group (P gt; 0.05). Whereas the thickness of myelin sheath in degenerated accellular nerve group was significantly less than that of autograft group (P lt; 0.05). CONCLUSION: The above results indicate that xenogeneic acellular nerve basal lamina scaffolds extracted by chemical procedure can be successfully used to repair nerve defects without any immunosuppressants.
Objective To investigate the promotion effect of neurotropic reinnervation with chemically extracted acellular nerve allograft. Methods The sciatic nerves of 5 healthy adult SD rats, regardless of gender and weighing 270-300 g, were collected to prepare chemically extracted acellular nerve allograft. Eighteen healthy adult Wistar rats, regardless of genderand weighing 300-320 g, were made the model of left sciatic nerve defect (10 mm) and randomly divided into 2 groups: autograft (control group, n=9) and allograft group (experimental group, n=9). The defects were bridged by acellular nerve allograft in experimental group and by autograft by turning over the proximal and distal ends of the nerve in control group. At 3 months after transplantation, dorsal root ganglion (DRG) resection operation was performed in 6 rats of 2 groups. At 3 weeks after operation, the sural nerves were harvested to calculate the misdirection rate of nerve fibers with pathological staining and compute-assisted image analysis. Cholinesterase staining and carbonic anhydrase staining were performed in the sural nerve of 3 rats that did not undergo DRG resection at 3 months. Results The results of chol inesterase staining and carbonic anhydrase staining showed that experimental group had less brown granules and more black granules than control group. After DRG resection, count of myelinated nerve fiber were 4 257 ± 285 in the experimental group and 4 494 ± 310 in the control group significant (P lt; 0.05). The misdirection rate was 2.27% ± 0.28% and 7.65% ± 0.68% in the experimental group and in the control group respectively, showing significant difference (P lt; 0.05). Conclusion Chemically extracted acellular nerve allograft can not only act as a scaffold in the period of nerve defects repair, but markedly enhance the effects of neurotropic reinnervation.
Objective To observe the revascularization process of chemically extracted acellular allogeneous nerve graft in repairing rat sciatic nerve defect. Methods Eighty adult male SD rats were selected. The sciatic nerve trunks from ischial tuberosity to the ramus of tibiofibular nerve of 16 SD rats were obtained and were prepared into acellular nerve stents by chemical reagent. Sixty-four SD rats were used to prepare the models of sciatic nerve defect (1.0 cm) and thereafter were randomized into two groups (n=32): experimental group in which acellular allogeneous nerve grafts were adopted and control group in which orthotopic transplantation of autologous nerve grafts were adopted. Postoperatively, the general conditions of all rats were observed, and the gross and ALP staining observation were conducted at 5, 7, 10, 14, 21, 28 days and 2, 3 months, respectively. Results All the incisions were healed by first intention. Trail ing status and toe’s dysfunction in extension happened to the right hindl imb of rats in two groups and were improved 6 weeks after operation. General observation showed that the grafts of two groups connected well to the nerves, with appearances similar to that of normal nerve. ALP staining demonstrated that the experimental group had no ingrowth of microvessel but the control group had ingrowth of microvessel 5 days after operation; the experimental group had ingrowth of microvessel but both groups had no microvessel 7 days after operation; few longitudinal microvessel throughout the grafts were observed in both groups 10, 14 and 21 days after operation; no obvious difference in capillary network of grafts was observed between two groups 28 days after operation; and the microvascular architecture of grafts in both groups were similar to that of normal nerve 2 and 3 months after operation. Conclusion When the chemically extracted allogeneous nerve graft is adopted to repair the peripheral nerve defect, new blood microvessels can grow into grafts timely and effectively.