微囊化神经组织联合脱细胞神经移植修复犬坐骨神经缺损

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目的了解微囊化神经组织与脱细胞神经联合移植桥接犬坐骨神经30mm缺损后腓肠肌的变化。方法将健康成年杂种犬12只随机分为A、B、C、D 4组(n=3):A组截取双侧坐骨神经行化学萃取制备脱细胞神经;B、C组使用脱细胞神经移植修复犬的坐骨神经30mm缺损, B组同时辅以微囊化神经组织移植;D组行自体神经移植修复缺损。术后定期观察术侧肢体运动功能恢复情况,6个月时检测神经移植段运动传导速度,并取术侧及健侧腓肠肌行琥珀酸脱氢酶(succinic dehydrogenase, SDH)、突触素和运动终板染色,以及取距远端吻合口以远1cm的坐骨神经神经行Masson、固蓝及NF-200染色。结果 B、C、D组实验动物均纳入实验动物数量分析、无脱失。图像分析表明B组腓肠肌SDH光密度、肌纤维截面积、突触素及运动终板光密度及面积等与C组有明显统计学差别,而与D组无明显统计学差别,运动功能恢复、电生理及坐骨神经形态学检测均与腓肠肌检测结果相符合。结论微囊化神经组织细胞与脱细胞神经联合移植修复缺损神经后,重新支配靶器官,使腓肠肌萎缩明显减弱,效果优于单纯脱细胞神经移植,有望代替自体神经移植。 Objective To investigate the changes of gastrocnemius muscle after 30 mm defect of canine sciatic nerve bridging with microencapsulated nerve tissue and acellular nerve. Methods Twelve healthy adult dogs were randomly divided into 4 groups (A, B, C, D 4): group A (group B) was prepared by chemical extraction of bilateral sciatic nerves; group B and C were treated with acellular nerve graft Canine sciatic nerve 30mm defect, while group B supplemented with microencapsulated nerve tissue transplantation; D group autologous nerve graft to repair the defect. The motor function recovery of the limbs was observed regularly. The motor conduction velocity of the nerve graft was detected at 6 months. The succinic dehydrogenase (SDH), synaptophysin and exercise Endplate staining, and Masson, solid blue and NF-200 staining of sciatic nerve nerves 1 cm distal to the distal anastomosis. Results The experimental animals in groups B, C and D were all included in the quantitative analysis of the experimental animals, without loss. Image analysis showed that optical density of SDH, cross-sectional area of ​​muscle fiber, optical density and area of ​​synaptophysin and motor endplate in group B were significantly different from those in group C, but there was no significant difference between group B and group D. Motor function recovered, Physiological and sciatic nerve morphological tests were consistent with gastrocnemius muscle test results. CONCLUSIONS: After the microencapsulated nerve tissue cells and acellular nerve are combined to repair the defect nerve, the target organs are re-dominating. The atrophy of the gastrocnemius muscle is obviously weakened, and the effect is better than that of pure acellular nerve transplantation. It is expected to replace autologous nerve graft.
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