本文選題：脊髓損傷　切入點：基質(zhì)金屬蛋白酶2　出處：《安徽醫(yī)科大學(xué)》2017年碩士論文　論文類型：學(xué)位論文

【摘要】：目的通過冠狀動脈成形(percutaneous transluminal coronary angioplasty,PTCA)球囊擴張導(dǎo)管技術(shù)制備新西蘭大白兔急性脊髓壓迫損傷模型,模擬胸腰椎爆裂骨折合并脊髓壓迫性損傷(spinal cord injury,SCI),探討損傷控制骨科(damage control orthopedics,DCO)策略手術(shù)治療兔重度脊髓壓迫性損傷的效果方法選擇清潔健康的雄性新西蘭大白兔45只,應(yīng)用PTCA球囊壓迫法制備新西蘭大白兔脊髓壓迫損傷模型,造模術(shù)后2d行減壓手術(shù),減壓手術(shù)前1h隨機取5只完成行為學(xué)觀測、評分后取出損傷區(qū)脊髓組織進(jìn)行流式細(xì)胞儀凋亡細(xì)胞檢測、病理學(xué)觀察、免疫組化染色檢測兔損傷區(qū)脊髓組織中基質(zhì)金屬蛋白酶2(matrix metalloproteinase-2,MMP-2)表達(dá)(對照組),剩余40只隨機分為兩組,每組20只,減壓術(shù)前,損傷控制組(DCO組,A組)先將球囊內(nèi)壓力減為原來一半,致使椎管內(nèi)有效容積增加后再自遠(yuǎn)離脊髓壓迫較重的一側(cè)進(jìn)行全椎板減壓。傳統(tǒng)手術(shù)組(B組)先予全椎板減壓,減壓自壓迫最嚴(yán)重部位開始,兩組減壓完畢后取出球囊,并在減壓術(shù)后1d、3d、7d、14d分別隨機取5只實驗兔完成以上檢測內(nèi)容。結(jié)果A、B組實驗兔減壓術(shù)后1d時Tarlov評分與對照組比較均無統(tǒng)計學(xué)差異(P0.05),且A、B組減壓術(shù)后1d、3d、7d Tarlov評分比較差異均無統(tǒng)計學(xué)意義(P0.05);減壓術(shù)后14d A組評分高于B組(P0.05)。減壓術(shù)后1d、3d,A、B兩組動物損傷區(qū)脊髓細(xì)胞凋亡率差異無統(tǒng)計學(xué)意義(P0.05),但A、B組減壓術(shù)后1d時其脊髓細(xì)胞凋亡率均低于對照組(P.05);A組減壓術(shù)后1d、3d,7d、14d損傷區(qū)脊髓細(xì)胞凋亡率差異無統(tǒng)計學(xué)意義(P0.05);B組減壓術(shù)后1d、3d,7d、14d損傷區(qū)脊髓細(xì)胞凋亡率差異亦無統(tǒng)計學(xué)意義(P0.05),但A組減壓術(shù)后3d、7d脊髓細(xì)胞凋亡率有統(tǒng)計學(xué)差異(P0.05);B組減壓術(shù)后3d、7d脊髓細(xì)胞凋亡率亦存在統(tǒng)計學(xué)差異(P0.05),且減壓術(shù)后7d、14d,A組細(xì)胞損傷區(qū)脊髓細(xì)胞凋亡率均低于同時間點B組(P0.05)。病理學(xué)觀察顯示:對照組白質(zhì)輕度脫髓鞘、部分軸突空泡樣變,灰質(zhì)內(nèi)細(xì)胞水腫,A、B組減壓術(shù)后1d、3d、7d、14d白質(zhì)彌漫性脫髓鞘改變及散在點狀出血,灰質(zhì)內(nèi)細(xì)胞水腫伴神經(jīng)細(xì)胞變性逐漸加重,至減壓術(shù)后7d時灰質(zhì)內(nèi)廣泛神經(jīng)細(xì)胞變性,并持續(xù)到術(shù)后14d。免疫組化結(jié)果顯示:減壓術(shù)后1d、3d、7d、14d時B組MMP-2表達(dá)陽性細(xì)胞率均高于A組(P0.05),且A組減壓術(shù)后3d、7d,7d、14d比較差異有統(tǒng)計學(xué)意義(P0.05),B組減壓術(shù)后3d、7d,7d、14d比較差異亦有統(tǒng)計學(xué)意義(P0.05),但A組減壓術(shù)后1d、3d比較無統(tǒng)計學(xué)差異(P0.05),B組減壓術(shù)后1d、3d比較亦無統(tǒng)計學(xué)差異(P0.05)。結(jié)論由于壓迫同側(cè)減壓手術(shù)減壓前椎管有效容積未增加且減壓自壓迫最嚴(yán)重部位開始,易對損傷脊髓造成繼發(fā)性損傷,建議對胸腰椎爆裂骨折合并脊髓壓迫損傷的治療采用DCO方案,療效滿意。
[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.
【學(xué)位授予單位】：安徽醫(yī)科大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2017
【分類號】：R651.2

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