Résumé
<p><b>OBJECTIVE</b>To study the changes of vascular endothelial cell function and platelet activation in rabbit spinal cord following ischemia-reperfusion (I/R) injury and their roles in the spinal cord injury.</p><p><b>METHODS</b>Rabbit spinal cord I/R injury models were established using Zivin method, and the changes in plasma NO and GMP140 levels were dynamically monitored after the injury.</p><p><b>RESULTS</b>Plasma NO level increased significantly in the I/R group at the end of the ischemia, and reached the peak level at 2 h of reperfusion as compared to that in sham-operated group (P<0.01). Plasma NO level decreased at 6 h of reperfusion, but still significantly higher than the level in the sham-operated group (P<0.05). Plasma GMP140 underwent no significant changes in the sham-operated group, but significantly increased in the I/R group at the end of the ischemia, followed by gradual declination to the normal level at 2 h of reperfusion.</p><p><b>CONCLUSION</b>Spinal cord I/R injury causes overexpressions of NO and GMP140, suggesting the involvement of endothelial cell injury and platelet overactivation in the pathological process and repair of spinal cord I/R injury.</p>