兔寰枢椎前脱位不全脊髓损伤早期细胞凋亡的实验研究

目的制备伴脊髓不全损伤兔寰枢椎前脱位模型,观察模型早期脊髓神经细胞凋亡的变化。方法建立伴脊髓不全损伤兔寰枢椎前脱位模型,采用原位末端转移酶标记技术（terminal deoxynucleotidyl transferase-mediatednick-end labeling,TUNEL）检测术后6 h、24 h、72 h损伤节段脊髓细胞的形态及数量变化。结果伤后6 h,损伤节段脊髓可见阳性神经细胞大量表达,至24 h损伤段阳性神经细胞达高峰,持续至72 h阳性神经细胞数见下降。各时间点与假手术组比较,损伤段脊髓神经细胞凋亡数均增加（P〈0.05）,凋亡的神经细胞数在24 h较6 h、72 h均更多（P〈0.05）。结论通过手术方式可成功制备寰枢椎前脱位并脊髓损伤模型,在模型寰枢椎可靠固定的前提下（未复位）,脊髓损伤逐渐加重,脊髓损伤后广泛存在细胞凋亡。

Early Neurocyte Apoptosis of Rabbits with Spinal Cord Injury Induced by Atlantoaxial Anterior Dislocation

Objective To establish the partial spinal cord injury model with atlantoaxial dislocation in rabbits by surgical operation and observe the early pathological changes of apoptotic death of neural cells.Methods The model of partial spinal cord injury induced by atlantoaxial anterior dislocation in rabbits was established.Terminal deoxynuleotidyl-mediated nick end labeling(TUNEL) was used to detect the expression of neuyocytic apoptosis in the injured site 6,24 and 72 hours after operation.Results A great number of TUNEL-positive cells were observed in the injured site at 6 hours after operation,reached the peak 24 hours after operation,and continued until 72 hours after operation.The numbers of the apoptosis neurocytes were increased compared with the sham-operated control group at all the timepoints(P<0.05).These numbers were higher at 24 hours after operation than those at 6 hours and 72 hours after operation(P<0.05).Conclusion Partial spinal cord injury model with atlantoaxial dislocation in rabbits can be successfully established by surgical operation.Spine cord injury gradually gets worse after reliable fixation of atlantoaxial(no reset) and the apoptosis of neural cells occur extensively.