腰椎间孔外口植入髓核致坐骨神经痛大鼠模型的建立

发布时间：2018-01-09 07:25

本文关键词：腰椎间孔外口植入髓核致坐骨神经痛大鼠模型的建立　出处：《北京中医药》2015年03期 　论文类型：期刊论文

【摘要】：目的建立一种新的腰椎间孔外口植入髓核致坐骨神经痛大鼠模型。方法 54只雄性SD大鼠随机分为模型组、假手术组和空白组各18只。每组各取6只于术前1天及术后第1、3、5、7、10、14天行一般行为学观察和50%机械性撤足痛阈值(PWT)的测定。另各取6只分别于术后第3和7天检测术侧L5背根神经节中NOS和COX-2的表达。结果所有大鼠均未出现运动功能明显障碍。模型组50%PWT在术后各观察时点比术前、空白组和假手术组均明显减低(P0.01)。模型组术侧L5背根神经节NOS和COX-2的阳性细胞数在术后第3和7天均较空白组和假手术组明显升高(P0.01)。结论本研究建立的椎间孔外口植入髓核致坐骨神经痛大鼠模型创伤小,制作简便,不破坏关节结构,神经根性疼痛确实、持续、稳定。该模型为脊柱关节手法等保守治疗神经根刺激的机制研究提供了实验基础。
[Abstract]:Objective to establish a new lumbar intervertebral outside foramen implant model in rats induced by nucleus pulposus sciatica. Methods 54 male SD rats were randomly divided into model group, sham operation group and control group with 18 rats in each group. Each group take 6 to 1 days before and after the first 1,3,5,7,10,14 days general behavioral observation and 50% mechanical paw withdrawal threshold of pain (PWT) determination. The other = 6 in each group were sacrificed at third and 7 days postoperatively L5 detection NOS and COX-2 dorsal root ganglia in expression. Results all the rats showed no obvious motor function disorder. 50%PWT model group after each observation point than before operation, control group and sham operation group were decreased significantly (P0.01). The number of positive cells in model group were side L5 NOS in dorsal root ganglion and COX-2 after third and 7 days compared with control group and sham operation group were significantly increased (P0.01). Conclusion the establishment of extraforaminal mouth model induced by implanting the nucleus sciatica in rats Small trauma, simple production, no damage to the joint structure, nerve root pain indeed, sustained, stable. This model provides the experimental basis for the research on the mechanism of spinal joint technique of conservative treatment of nerve root stimulation.

【作者单位】：中国人民解放军空军总医院脊柱正骨中心;
【基金】：中国博士后科学基金资助项目(2014M552662)
【分类号】：R-332;R745.42
【正文快照】： 腰椎间盘突出症(以下简称腰突症)是导致成年劳动者腰腿痛最常见的原因之一,据估计成人年发生率约为5‰[1-2]。罹患者会感知不同程度的急性或慢性疼痛,还会伴随生活功能的部分障碍,尤其在急性期更为显著。目前较为公认的发病机制之一是突出髓核突冲破椎间盘纤维环束缚而引起邻

【参考文献】