损伤控制骨科应用于手术治疗脊髓损伤的实验研究

发布时间：2018-03-18 15:05

本文选题：脊髓损伤　切入点：基质金属蛋白酶2　出处：《安徽医科大学》2017年硕士论文　论文类型：学位论文

【摘要】：目的通过冠状动脉成形(percutaneous transluminal coronary angioplasty,PTCA)球囊扩张导管技术制备新西兰大白兔急性脊髓压迫损伤模型,模拟胸腰椎爆裂骨折合并脊髓压迫性损伤(spinal cord injury,SCI),探讨损伤控制骨科(damage control orthopedics,DCO)策略手术治疗兔重度脊髓压迫性损伤的效果方法选择清洁健康的雄性新西兰大白兔45只,应用PTCA球囊压迫法制备新西兰大白兔脊髓压迫损伤模型,造模术后2d行减压手术,减压手术前1h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(matrix metalloproteinase-2,MMP-2)表达(对照组),剩余40只随机分为两组,每组20只,减压术前,损伤控制组(DCO组,A组)先将球囊内压力减为原来一半,致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。传统手术组(B组)先予全椎板减压,减压自压迫最严重部位开始,两组减压完毕后取出球囊,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A、B组实验兔减压术后1d时Tarlov评分与对照组比较均无统计学差异(P0.05),且A、B组减压术后1d、3d、7d Tarlov评分比较差异均无统计学意义(P0.05);减压术后14d A组评分高于B组(P0.05)。减压术后1d、3d,A、B两组动物损伤区脊髓细胞凋亡率差异无统计学意义(P0.05),但A、B组减压术后1d时其脊髓细胞凋亡率均低于对照组(P.05);A组减压术后1d、3d,7d、14d损伤区脊髓细胞凋亡率差异无统计学意义(P0.05);B组减压术后1d、3d,7d、14d损伤区脊髓细胞凋亡率差异亦无统计学意义(P0.05),但A组减压术后3d、7d脊髓细胞凋亡率有统计学差异(P0.05);B组减压术后3d、7d脊髓细胞凋亡率亦存在统计学差异(P0.05),且减压术后7d、14d,A组细胞损伤区脊髓细胞凋亡率均低于同时间点B组(P0.05)。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。免疫组化结果显示:减压术后1d、3d、7d、14d时B组MMP-2表达阳性细胞率均高于A组(P0.05),且A组减压术后3d、7d,7d、14d比较差异有统计学意义(P0.05),B组减压术后3d、7d,7d、14d比较差异亦有统计学意义(P0.05),但A组减压术后1d、3d比较无统计学差异(P0.05),B组减压术后1d、3d比较亦无统计学差异(P0.05)。结论由于压迫同侧减压手术减压前椎管有效容积未增加且减压自压迫最严重部位开始,易对损伤脊髓造成继发性损伤,建议对胸腰椎爆裂骨折合并脊髓压迫损伤的治疗采用DCO方案,疗效满意。
[Abstract]:Objective to establish a new Zealand white rabbit model of acute spinal cord compression injury by percutaneous transluminal coronary balloon dilation catheter. Simulated thoracolumbar burst fracture combined with spinal cord compression injury (cord injurys), the purpose of this study was to investigate the effect of surgical treatment of severe spinal cord compression injury in rabbits using orthopedic control orthopedics in orthopedic department. 45 healthy and clean male New Zealand white rabbits were selected. The spinal cord compression injury model of New Zealand white rabbits was established by PTCA balloon compression. Decompression was performed 2 days after operation. 5 rabbits were randomly selected 1 hour before decompression. After scoring, the spinal cord tissues were taken out for flow cytometry, pathological observation and immunohistochemical staining to detect the expression of matrix metalloproteinase-2 matrix metalloproteinase-2 (MMP-2) in the injured spinal cord of rabbits (control group, the remaining 40 rats were randomly divided into two groups). 20 rats in each group, before decompression, the injury control group was treated with DCO group A) the balloon pressure was reduced to half. As a result, the effective volume of the spinal canal was increased and then decompressed from the side of the spinal cord. The traditional operation group (group B) was treated with total lamina decompression first, the decompression began at the most severe part of the spinal canal, and the balloon was removed after decompression in both groups. The results showed that there was no significant difference in Tarlov score between group A and group B at 1 day after decompression and control group (P 0.05), and the Tarlov score of group A B was worse than that of group A on day 3 and day 7 after decompression. On the 14th day after decompression, the score of group A was higher than that of group B (P 0.05). There was no significant difference in apoptotic rate of spinal cord cells between the two groups on the 1st day after decompression, but the apoptotic rate of spinal cord cells in group A was lower than that in group A at 1 day after decompression. There was no significant difference in the apoptosis rate of spinal cord cells in the control group 1 day after decompression 3 days and 7 days and 14 days after decompression. There was no significant difference in apoptosis rate of spinal cord cells between group A and group B on the 1st day, 3rd day, 7th day, 14 day after decompression, but there was no significant difference in apoptosis rate of spinal cord cells in group A on 3 days after decompression and 7 days after decompression, but in group A there was no significant difference in apoptotic rate of spinal cord cells at 3 days after decompression and 7 days after decompression. There was significant difference in the rate of apoptosis of spinal cord cells between group B and group B on the 3rd day after decompression, and the apoptosis rate of spinal cord cells in group A was lower than that in group B at 7 days after decompression. The pathological observation showed that the apoptosis rate of spinal cord cells in group A was lower than that in group B at the same time point. The pathological observation showed that the apoptosis rate of spinal cord cells in group A was lower than that in group B at 7 days after decompression. Mildly demyelinating white matter, Some axonal vacuolation and edema in gray matter were observed in group A (1 d ~ 3 d ~ 7 d ~ 14 d after decompression) and diffuse demyelination of white matter and scattered hemorrhage. The edema of cells in gray matter accompanied with degeneration of nerve cells was gradually aggravated. By 7 days after decompression, extensive degeneration of nerve cells in gray matter was observed. The results of immunohistochemistry showed that the positive rate of MMP-2 expression in group B was higher than that in group A at 1 day, 3 days and 7 days after decompression, and there was a significant difference between group A and group B on the 3rd day, 7th day and 14th day after decompression. There was also a significant difference between group B and group B on the 3rd day, 7th day, 7d and 14d after decompression. There was no statistical difference between group A and group B at 1 day after decompression. Conclusion the effective volume of vertebral canal before decompression in ipsilateral decompression did not increase and the decompression began at the most severe part of decompression. The treatment of thoracolumbar burst fracture combined with spinal cord compression injury is easy to cause secondary injury. The therapeutic effect is satisfactory.
【学位授予单位】：安徽医科大学
【学位级别】：硕士
【学位授予年份】：2017
【分类号】：R651.2

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