Ischemic preconditioning to prevent lethal ischemic spinal cord injury in a swine model
- Authors
- Lee, Jeong-Sang; Hong, Jong-Myeon; Kim, Yong-Joo
- Issue Date
- Jul-2008
- Publisher
- TAYLOR & FRANCIS INC
- Keywords
- ischemic injury; spinal cord; ischemic preconditioning
- Citation
- JOURNAL OF INVESTIGATIVE SURGERY, v.21, no.4, pp.209 - 214
- Indexed
- SCIE
SCOPUS
- Journal Title
- JOURNAL OF INVESTIGATIVE SURGERY
- Volume
- 21
- Number
- 4
- Start Page
- 209
- End Page
- 214
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/178160
- DOI
- 10.1080/08941930802262249
- ISSN
- 0894-1939
- Abstract
- Objective: Paraplegia is a serious complication of thoracic and thoracoabdominal aortic operations and is the result of ischemic spinal cord injury induced by low perfusion pressure during cross-clamping of the aorta. Ischemic preconditioning (IPC) of the heart or brain with reversible sublethal ischemic injury induces resistance to subsequent lethal ischemia. The aim of this study is to investigate whether ischemic tolerance can be induced by IPC of the spinal cord in a swine model. Study Design: The animals were randomly divided into three groups: the sham group (n = 3), control group (n = 6) and IPC group (n = 8). In the sham group, we performed a left thoracotomy without any ischemic injury. In the IPC group, the swine received a reversible ischemic spinal cord injury by aortic clamping for 20 min, whereas in the control group, no aortic cross-clamping was performed. Forty-eight hours later, the animals in both the IPC and control groups underwent aortic clamping for 30 min. Neurological examination was done 24 h later, and then the animals were euthanized for histopathology and a malonedialdehyde spectrophotometry assay of the spinal cord tissue. Results: A statistically significant difference in neurological outcome was observed between the control and IPC groups at 24 h after ischemic injury. The incidence of paraplegia and severe paresis was 100% in the control group and 62.5% in the IPC group (p = .028). Between control and IPC groups, there was no statistically significant difference in histopathology and only a borderline statistical difference in the malonedialdehyde assay of the ischemic spinal cord (p = .0745). Conclusion: In this study, IPC induced protection against a 30-min ischemic insult of the spinal cord, although complete recovery was not achieved (standing up or walking). We expect that combining this IPC with other existing protective methods might lead to a synergistic effect, which warrants further investigation.
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