Ischemia–reperfusion injury after spinal cord decompressive surgery—An in vivo rat model
Abstract Background Although decompression surgery is the optimal treatment for patients with severe degenerative cervical myelopathy (DCM), some individuals experience no improvement or even a decline in neurological function after surgery, with spinal cord ischemia–reperfusion injury (SCII) identi...
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Wiley
2025-03-01
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| Series: | Animal Models and Experimental Medicine |
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| Online Access: | https://doi.org/10.1002/ame2.12485 |
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| author | Boyu Zhang Zhefeng Jin Pengren Luo He Yin Xin Chen Bowen Yang Xiaokuan Qin LiGuo Zhu Bo Xu Guoliang Ma Dian Zhang |
| author_facet | Boyu Zhang Zhefeng Jin Pengren Luo He Yin Xin Chen Bowen Yang Xiaokuan Qin LiGuo Zhu Bo Xu Guoliang Ma Dian Zhang |
| author_sort | Boyu Zhang |
| collection | DOAJ |
| description | Abstract Background Although decompression surgery is the optimal treatment for patients with severe degenerative cervical myelopathy (DCM), some individuals experience no improvement or even a decline in neurological function after surgery, with spinal cord ischemia–reperfusion injury (SCII) identified as the primary cause. Spinal cord compression results in local ischemia and blood perfusion following decompression is fundamental to SCII. However, owing to inadequate perioperative blood flow monitoring, direct evidence regarding the occurrence of SCII after decompression is lacking. The objective of this study was to establish a suitable animal model for investigating the underlying mechanism of spinal cord ischemia–reperfusion injury following decompression surgery for degenerative cervical myelopathy (DCM) and to elucidate alterations in neurological function and local blood flow within the spinal cord before and after decompression. Methods Twenty‐four Sprague–Dawley rats were allocated to three groups: the DCM group (cervical compression group, with implanted compression material in the spinal canal, n = 8), the DCM‐D group (cervical decompression group, with removal of compression material from the spinal canal 4 weeks after implantation, n = 8), and the SHAM group (sham operation, n = 8). Von Frey test, forepaw grip strength, and gait were assessed within 4 weeks post‐implantation. Spinal cord compression was evaluated using magnetic resonance imaging. Local blood flow in the spinal cord was monitored during the perioperative decompression. The rats were sacrificed 1 week after decompression to observe morphological changes in the compressed or decompressed segments of the spinal cord. Additionally, NeuN expression and the oxidative damage marker 8‐oxoG DNA were analyzed. Results Following spinal cord compression, abnormal mechanical pain worsened, and a decrease in forepaw grip strength was observed within 1–4 weeks. Upon decompression, the abnormal mechanical pain subsided, and forepaw grip strength was restored; however, neither reached the level of the sham operation group. Decompression leads to an increase in the local blood flow, indicating improved perfusion of the spinal cord. The number of NeuN‐positive cells in the spinal cord of rats in the DCM‐D group exceeded that in the DCM group but remained lower than that in the SHAM group. Notably, a higher level of 8‐oxoG DNA expression was observed, suggesting oxidative stress following spinal cord decompression. Conclusion This model is deemed suitable for analyzing the underlying mechanism of SCII following decompressive cervical laminectomy, as we posit that the obtained results are comparable to the clinical progression of degenerative cervical myelopathy (DCM) post‐decompression and exhibit analogous neurological alterations. Notably, this model revealed ischemic reperfusion in the spinal cord after decompression, concomitant with oxidative damage, which plausibly underlies the neurological deterioration observed after decompression. |
| format | Article |
| id | doaj-art-b0ea85f7a3a4413ba32d4700cbc6fc61 |
| institution | OA Journals |
| issn | 2576-2095 |
| language | English |
| publishDate | 2025-03-01 |
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| series | Animal Models and Experimental Medicine |
| spelling | doaj-art-b0ea85f7a3a4413ba32d4700cbc6fc612025-08-20T02:04:51ZengWileyAnimal Models and Experimental Medicine2576-20952025-03-018340542010.1002/ame2.12485Ischemia–reperfusion injury after spinal cord decompressive surgery—An in vivo rat modelBoyu Zhang0Zhefeng Jin1Pengren Luo2He Yin3Xin Chen4Bowen Yang5Xiaokuan Qin6LiGuo Zhu7Bo Xu8Guoliang Ma9Dian Zhang10Sports medicine department 3 Wangjing Hospital Affiliated to China Academy of Chinese Medical Sciences Beijing ChinaSports medicine department 3 Wangjing Hospital Affiliated to China Academy of Chinese Medical Sciences Beijing ChinaSports medicine department 3 Wangjing Hospital Affiliated to China Academy of Chinese Medical Sciences Beijing ChinaSpine Department 2 Wangjing Hospital Affiliated to China Academy of Chinese Medical Sciences Beijing ChinaSpine Department 2 Wangjing Hospital Affiliated to China Academy of Chinese Medical Sciences Beijing ChinaSpine Department 2 Wangjing Hospital Affiliated to China Academy of Chinese Medical Sciences Beijing ChinaSpine Department 2 Wangjing Hospital Affiliated to China Academy of Chinese Medical Sciences Beijing ChinaSports medicine department 3 Wangjing Hospital Affiliated to China Academy of Chinese Medical Sciences Beijing ChinaSpine Department 2 Wangjing Hospital Affiliated to China Academy of Chinese Medical Sciences Beijing ChinaSpine Department 2 Wangjing Hospital Affiliated to China Academy of Chinese Medical Sciences Beijing ChinaSpine Department 2 Wangjing Hospital Affiliated to China Academy of Chinese Medical Sciences Beijing ChinaAbstract Background Although decompression surgery is the optimal treatment for patients with severe degenerative cervical myelopathy (DCM), some individuals experience no improvement or even a decline in neurological function after surgery, with spinal cord ischemia–reperfusion injury (SCII) identified as the primary cause. Spinal cord compression results in local ischemia and blood perfusion following decompression is fundamental to SCII. However, owing to inadequate perioperative blood flow monitoring, direct evidence regarding the occurrence of SCII after decompression is lacking. The objective of this study was to establish a suitable animal model for investigating the underlying mechanism of spinal cord ischemia–reperfusion injury following decompression surgery for degenerative cervical myelopathy (DCM) and to elucidate alterations in neurological function and local blood flow within the spinal cord before and after decompression. Methods Twenty‐four Sprague–Dawley rats were allocated to three groups: the DCM group (cervical compression group, with implanted compression material in the spinal canal, n = 8), the DCM‐D group (cervical decompression group, with removal of compression material from the spinal canal 4 weeks after implantation, n = 8), and the SHAM group (sham operation, n = 8). Von Frey test, forepaw grip strength, and gait were assessed within 4 weeks post‐implantation. Spinal cord compression was evaluated using magnetic resonance imaging. Local blood flow in the spinal cord was monitored during the perioperative decompression. The rats were sacrificed 1 week after decompression to observe morphological changes in the compressed or decompressed segments of the spinal cord. Additionally, NeuN expression and the oxidative damage marker 8‐oxoG DNA were analyzed. Results Following spinal cord compression, abnormal mechanical pain worsened, and a decrease in forepaw grip strength was observed within 1–4 weeks. Upon decompression, the abnormal mechanical pain subsided, and forepaw grip strength was restored; however, neither reached the level of the sham operation group. Decompression leads to an increase in the local blood flow, indicating improved perfusion of the spinal cord. The number of NeuN‐positive cells in the spinal cord of rats in the DCM‐D group exceeded that in the DCM group but remained lower than that in the SHAM group. Notably, a higher level of 8‐oxoG DNA expression was observed, suggesting oxidative stress following spinal cord decompression. Conclusion This model is deemed suitable for analyzing the underlying mechanism of SCII following decompressive cervical laminectomy, as we posit that the obtained results are comparable to the clinical progression of degenerative cervical myelopathy (DCM) post‐decompression and exhibit analogous neurological alterations. Notably, this model revealed ischemic reperfusion in the spinal cord after decompression, concomitant with oxidative damage, which plausibly underlies the neurological deterioration observed after decompression.https://doi.org/10.1002/ame2.124858‐oxoG DNAdegenerative cervical myelopathyspinal cord ischemia–reperfusion injurysurgical decompression |
| spellingShingle | Boyu Zhang Zhefeng Jin Pengren Luo He Yin Xin Chen Bowen Yang Xiaokuan Qin LiGuo Zhu Bo Xu Guoliang Ma Dian Zhang Ischemia–reperfusion injury after spinal cord decompressive surgery—An in vivo rat model Animal Models and Experimental Medicine 8‐oxoG DNA degenerative cervical myelopathy spinal cord ischemia–reperfusion injury surgical decompression |
| title | Ischemia–reperfusion injury after spinal cord decompressive surgery—An in vivo rat model |
| title_full | Ischemia–reperfusion injury after spinal cord decompressive surgery—An in vivo rat model |
| title_fullStr | Ischemia–reperfusion injury after spinal cord decompressive surgery—An in vivo rat model |
| title_full_unstemmed | Ischemia–reperfusion injury after spinal cord decompressive surgery—An in vivo rat model |
| title_short | Ischemia–reperfusion injury after spinal cord decompressive surgery—An in vivo rat model |
| title_sort | ischemia reperfusion injury after spinal cord decompressive surgery an in vivo rat model |
| topic | 8‐oxoG DNA degenerative cervical myelopathy spinal cord ischemia–reperfusion injury surgical decompression |
| url | https://doi.org/10.1002/ame2.12485 |
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