损伤控制手术治疗兔脊髓压迫性损伤的效果

Damage control orthopedics for spinal cord compression injury in rabbits

中文关键词:  脊髓损伤  基质金属蛋白酶2  细胞凋亡  流式细胞仪  损伤控制手术

英文关键词:Spinal cord injury  Matrix metallopeptidase-2  Apoptosis  Flow cytometry  Damage control operation

中文摘要:

  【摘要】 目的：探讨损伤控制手术（damage control operation）治疗兔脊髓压迫性损伤的效果。方法：应用球囊压迫法制备新西兰大白兔脊髓压迫损伤模型45只，造模术后2d随机取5只完成行为学观测、评分后取出损伤区脊髓组织进行流式细胞仪凋亡细胞检测、病理学观察、免疫组化染色检测兔损伤区脊髓组织中基质金属蛋白酶2（MMP-2）表达（对照组），剩余40只随机分为两组，每组20只，一组采用损伤控制手术（A组），即减压术前先将球囊内压力减为原来一半，使椎管内有效容积增加后再自远离脊髓压迫较重的一侧进行全椎板减压；另一组直接予全椎板切除减压，减压自压迫最严重部位开始（B组），两组减压完毕后均取出球囊，并在减压术后1d、3d、7d、14d分别随机取5只实验兔完成以上检测内容。结果：对照组造模术后48h的Tarlov评分为1.20±0.45分，A、B组减压术后1d时Tarlov评分与对照组比较均无统计学差异（P＞0.05）；A、B组减压术后1d、3d、7d时的 Tarlov评分均无统计学差异（P>0.05），减压术后14d时A组高于B组（P<0.05）。对照组脊髓细胞凋亡率为（2.66±1.40）%，A、B组减压术后1d时脊髓细胞凋亡率均低于对照组（P＜0.05）；减压术后1d、3d时A、B两组损伤区脊髓细胞凋亡率无统计学差异（P>0.05）；A、B组减压术后1d与3d、7d与14d损伤区脊髓细胞凋亡率无统计学差异（P>0.05）；A、B组减压术后3d与7d损伤区脊髓细胞凋亡率均有统计学差异（P<0.05）；减压术后7d、14d时A组损伤区脊髓细胞凋亡率均低于同时间点B组（P<0.05）。病理学观察显示对照组白质轻度脱髓鞘、部分轴突空泡样变，灰质内细胞水肿，A、B组减压术后1d、3d、7d、14d白质弥漫性脱髓鞘改变及散在点状出血，灰质内细胞水肿伴神经细胞变性逐渐加重，至减压术后7d时灰质内广泛神经细胞变性，并持续到术后14d。对照组MMP-2表达阳性细胞率为（45.76±0.75）%，A、B组减压术后1d时MMP-2表达阳性率均低于对照组（P＜0.05）；减压术后1d、3d、7d、14d时B组MMP-2表达阳性细胞率均高于同时间点A组（P<0.05），A、B组减压术后1d、3d比较均无统计学差异（P>0.05），3d、7d，7d、14d比较均有统计学差异（P<0.05）。结论：损伤控制手术治疗兔脊髓压迫性损伤较直接减压效果好，建议对胸腰椎爆裂骨折合并脊髓压迫损伤的治疗采用损伤控制手术方案。

英文摘要:

  【Abstract】 Objectives: To investigate the operation procedures and outcomes of damage control operation for spinal cord compression injury in rabbits. Methods: The animal models of spinal cord compression injury were established by balloon compression in 45 white New Zealand rabbits. Decompression began 2 days after the first operation. 5 rabbits were randomly selected from the 45 models to carry on the following researches two hours after operation(control group): behavioral science, apoptotic spinal cord cells detected by flow cytometry, and expression of matrix metallopeptidase-2(MMP-2) detected by histopathological and immunohistochemical staining. The remaining 40 rabbits were randomly divided into 2 groups, 20 cases in each group. In the first group, the total laminectomy began far from the heavy oppressed side of spinal cord after balloon pressure reduced to half(contralateral decompression group, group A). In the second group, the whole vertebral plate was resected from the heavily oppressed side(ipsilateral decompression group, group B). Then the balloons were took out after decompression in the 2 groups. 5 rabbits were randomly and respectively taken from the 2 groups at 1d, 3d, 7d, 14d after decompression to complete the above test contents. Results: The differences of improved Tarlov motor function grades were not statistically significant between control group and group A or B at 1d after decompression(P>0.05). The differences of improved Tarlov motor function grades were not statistically significant between group A and B at 1d, 3d, 7d of post-decompression(P>0.05).　The improved Tarlov motor function grade test in group A was significantly improved compared with that in group B at 14d after decompression(P<0.05). No significant difference was found with respect to the apoptosis between group A and B(P>0.05) at 1d, 3d after decompression. The apoptosis was lower in group A and B at 1d of post-decompression than control group(P<0.05). The difference of the apoptosis was not statistically significant between 1d and 3d of post-decompression and between 7d and 14d of post-decompression in group A(P>0.05) and the same as in group B(P>0.05). However, the apoptosis was higher at 7d than at 3d post-decompression in group A(P<0.05) and the same as in group B(P<0.05). In addition, the apoptosis was lower in group A than group B at 7d and 14d after decompression(P<0.05). HE staining in control group showed mild demyelination changes and vacuolar degeneration in white matter company with nerve cell edema and neuron atrophy in gray matter. The injury of spinal cord at 1d, 3d, 7d and 14d after decompression in group A and B showed nerve cell edema company with degeneration in gray matter until pathological changes deteriorated at 7d after decompression, and maintained the changes to 14d after decompression. The diffuse demyelination changes company with dotted hemorrhage was showed in white matter. The immunohistochemical staining method to detect expression of MMP-2 in rabbits showed that the expression of MMP-2 in group B was significantly higher than that in group A(P<0.05). The expression of MMP-2 was lower in group A and B at 1d of post-decompression than in contol group(P<0.05). The expression of MMP-2 was higher at 3d than that in 7d of post-decompression and the expression was higher at 7d than that at 14d of post-decompression in group A and the same as in group B(P<0.05). However, no significant difference was found with respect to the expression of MMP-2 between 1d and 3d of post-decompression in group A(P>0.05) and the same as in group B(P>0.05). Conclusions: Ipsilateral decompression decompresses from the heavy oppressed side of spinal cord without increasing the effective volume of spinal canal, which easily causes the second spinal cord injury. Damage control operation is more effective than ipsilateral decompression in thoracolumbar burst fracture that causes spinal cord oppression and injury.