Persistent oppression and simple decompression both exacerbate spinal cord ascorbate levels
Persistent oppression and simple decompression both exacerbate spinal cord ascorbate levels
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DOI：
10.7150/ijms.41289
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发表时间：
2020-05
影响因子：
3.6
通讯作者：
Yawen Zhang;G. Hou;Wenliang Ji;F. Rao;Rubing Zhou;Shan Gao;L. Mao;Fang Zhou
中科院分区：
文献类型：
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作者：
Yawen Zhang;G. Hou;Wenliang Ji;F. Rao;Rubing Zhou;Shan Gao;L. Mao;Fang Zhou
背景：急性脊髓损伤后手术减压已成为骨科医生的共识。然而，急性脊髓损伤后手术减压时间窗的选择一直是骨科界最具争议的话题之一。目的：我们应用在线电化学系统（OECS）连续监测大鼠脊髓的抗坏血酸，以确定抗坏血酸水平受挫伤或持续压迫的影响程度。方法：成年Sprague-Dawley大鼠（n=10），采用抗坏血酸浓度记录仪记录T11跌落性脊髓损伤（SCI）。A组（n=5）脊髓损伤后立即减压。B组（n=5），伤后1 h开始挫伤压迫;结果如下：脊髓挫伤后即刻抗坏血酸水平升高，伤后60 min达1.62 μmol/L ± 0.61 μmol/L，为基础水平的217.30% ± 95.09%。与A组相比，B组抗坏血酸水平在伤后1h显著升高，达3.76 μmol/L ± 1.75 μmol/L，为基础水平的430.25% ± 101.30%。同时发现，持续加压1h后再减压，抗坏血酸峰值延迟，达5.71 μmol/L ± 2.69 μmol/L（基础值的627.73% ± 188.11%）。结论：我们的研究提供了第一手的直接实验证据表明抗坏血酸直接参与继发性脊髓损伤，并表现出脊髓连续压迫损伤后微环境变化的动态时程。
Background: Surgical decompression after acute spinal cord injury has become the consensus of orthopaedic surgeons. However, the choice of surgical decompression time window after acute spinal cord injury has been one of the most controversial topics in orthopaedics. Objective: We apply an online electrochemical system (OECS) for continuously monitoring the ascorbate of the rats' spinal cord to determine the extent to which ascorbate levels were influenced by contusion or sustained compression. Methods: Adult Sprague-Dawley rats (n=10) were instrumented for ascorbate concentration recording and received T11 drop spinal cord injury (SCI). The Group A (n=5) were treated with immediately decompression after SCI. The Group B (n=5) were contused and oppressed until 1 h after the injury to decompress. Results: The ascorbate level of spinal cord increased immediately by contusion injury and reached to 1.62 μmol/L ± 0.61 μmol/L (217.30% ± 95.09% of the basal level) at the time point of 60 min after the injury. Compared with the Group A, the ascorbate level in Group B increased more significantly at 1 h after the injury, reaching to 3.76 μmol/L ± 1.75 μmol/L (430.25% ± 101.30% of the basal level). Meanwhile, we also found that the decompression after 1 hour of continuous compression will cause delayed peaks of ascorbate reaching to 5.71 μmol/L ± 2.69 μmol/L (627.73% ± 188.11% of the basal level). Conclusion: Our study provides first-hand direct experimental evidence indicating ascorbate is directly involved in secondary spinal cord injury and exhibits the dynamic time course of microenvironment changes after continuous compression injury of the spinal cord.