| Objects: To observe the change which was caused by the delayed protection of ischemic preconditioning (IPC) on the neurological functions, histopathologic outcome and expression of HSP70 in rabbit spinal cord suffering from ischemic/reperfusion. To investigate the late phase of IPC on the apoptosis of neurons and expression of HSP70. To study the role IPC plays in delayed protection of spinal cord , which will be helpful to provide theoretical evidence for clinical treatment in the future. Methods: The spinal cord ischemia/reperfusion model of rabbit was made by clamping the infrarenal aortic of rabbits. The rabbits were randomly divided into the sham group (n=5), ischemia group (n=30) and IPC group (n=30). The sham group was anaesthetized and subjected to operation without abdominal aortic occlusion.In the ischemia group, the abdominal aortic was occluded for 35 minutes and then reperfused. The IPC group underwent three cycles of 5 minutes of abdominal aortic occlusion, 10 minutes reperfusion and 35 minutes of ischemia after 48 hours. Neurological outcome was scored after reperfusion. Then animals were killed at 8h,12h,24h,48h,7d after reperfusion and the spinal cords (L2-5) were removed for histopathologic examination, including hematoxylin and eosin staining and terminal deoxynucleotidyltrans-emediated dUTP-biotin nick end-labeling (TUNEL) staining method ,and measuring the expression of HSP70 by SP method in IPC group and ischemia group. Results: In ischemia group, there were severe paralyses in most of rabbits.HE staining showed few normal neurons at each point.A few scattered cells in the gray matter and white matter were positive for TUNEL staining 8h after ischemia.The number of TUNEL-positive cells reached a peak at 24h and decreased at 48h.There were a few cells expressing HSP70 at 8h and 12h,then disappeared at 24h.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 < 0.01).The variance of the numbers of apoptosis neurons were similar with those in ischemia group,but much less in number in IPC group at the same points.There were a lot of neurons expressing HSP70 at 8h and 12h,and still existed at 48h. Conclusion: Neuronal apoptosis may be an important mode of celluar death in the process of spinal cord ischemia/reperfusion injury.IPC protects spinal cord function from ischemia injury by an endogenous cellular protective mechanism.The mechanism of delayed protective function may relate to reducing apoptosis and adding the expression of HSP70.
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