Int J Med Sci 2020; 17(9):1167-1176. doi:10.7150/ijms.41289 This issue

Research Paper

Persistent oppression and simple decompression both exacerbate spinal cord ascorbate levels

Yawen Zhang1,2, Guojin Hou1, Wenliang Ji2, Feng Rao3, Rubing Zhou1, Shan Gao1, Lanqun Mao2,✉, Fang Zhou1,✉

1. Department of Orthopaedics, Peking University Third Hospital, Beijing, China
2. Beijing National Laboratory for Molecular Sciences, Institute of Chemistry, The Chinese Academy of Sciences (CAS), Beijing, China
3. Trauma Medicine Centre, Peking University People's Hospital, Beijing, China

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Zhang Y, Hou G, Ji W, Rao F, Zhou R, Gao S, Mao L, Zhou F. Persistent oppression and simple decompression both exacerbate spinal cord ascorbate levels. Int J Med Sci 2020; 17(9):1167-1176. doi:10.7150/ijms.41289. Available from

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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.

Keywords: Online electrochemical system, In vivo microdialysis, Ascorbate, Spinal cord injury