| Objects: To observe the change of ischemic preconditioning (IPC) on the locomotor functions, histopathologic outcome and levels of interleukin-8(IL-8) in rabbits spinal cord suffering from ischemic/reperfusion. To investigate the effect of IPC on the apoptosis of neurons and inflammation. To study the role and mechanism how IPC protect spinal cord function, which will be helpful to provide theory evidence for clinical treatment in the future.Methods: The spinal cord ischemia/reperfusion model was made by clamping the uifrarenal aortic in rabbits. 86 rabbits were divided into 2 experimental groups: group A for investigation by means of histologic study (n=43) and group B for immunochemical study (n=43). In group A, the rabbits were randomly divided into the sham group (n=3), IPC group (n=20) and ischemia group (n=20). The sham group was anaesthetized and subjected to operation without abdominal aortic occlusion. The IPC group had 5 minutes of abdominal aortic occlusion, 15 minutes reperfiision and 40 minutes of ischemia. In the ischemia group, the abdominal aortic was occlusion for 40 minutes and then reperfusion. Neurological outcome was scored after reperfusion. Then animals were sacrificed at 4h, 8h, 24h, 48h,7d after reperftision and the spinal cord (L2-5) was removed for histopathologic examination, including hematoxyiin and eosin staining and terminal deoxynucleotidyltrans-emediated dUTP-biotin nick end-labeling (TUNEL) staining method in IPC group and ischemia group. In group E, using the same model and protocol, the spinal cord was removed at 4tu 8rK 12ru 24tu 48h after reperfusion. The spinal IL-8 levels were measured by enzyme-linked-immunosorbent assay (ELASA) method. Results: In ischemia group, there were severity paralyses in most of rabbits. A few scattered cells in the gray matter and white matter were positive for TNUEL staining 8h after ischemia. The number of TUNEL-positive cells reached a peak at 24h and decreased at 48h. Spinal IL-8 levels increased significantly at 8h after reperfusion, reached a peak at 12h and decreased little by little. In IPC group, the neurological function scores at all time points were significantly higher than those in ischemia group (P < 0.01). There were more normal neurons in the anterior horn of the spinal cord in IPC group (P < 0.05). The tendency of change in spinal IL-8 levels and the numbers of apoptosis neurons were similar with those in ischemia group, but their levels were significantly decreased in IPC group at same points.Conclusion: Neuronal apoptosis and inflammation may be induced or aggravated in the process of spinal cord ischemia/reperfusion injury. IPCprotects spinal cord function from ischemia injury by an endogenous cellular protective mechanism. The mechanism of protective effects may be related to reducing apoptosis and inhibiting inflammation. |