OBJECTIVETo 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.

METHODSRabbit 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.

RESULTSPlasma 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.

CONCLUSIONSpinal 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.

Animals ; Endothelial Cells ; metabolism ; Nitric Oxide ; blood ; P-Selectin ; blood ; Platelet Activation ; Rabbits ; Reperfusion Injury ; blood ; pathology ; physiopathology ; Spinal Cord ; pathology ; physiopathology

Objective To observe the changes in serum and spinal cord nitric oxide (NO) levels after spinal cord ischemia-reperfusion (IR) injury in rabbits. Methods The Zivin method was used to induce spinal cord IR injury in rabbits, in which the NO levels in the serum and spinal cord tissues were observed dynamically. Results In rabbits with spinal cord IR injury, the serum NO levels increased gradually after spinal cord IR injury and reached a peak level at 2 h, showing significant difference from the levels of before ischemia (P<0.05), and followed by obvious reduction at 6 and 12 h after the injury (P<0.05). In the spinal cord tissue homogenate, the NO levels increased significantly to reach the peak level at the end of the ischemia (P<0.05), and then decreased obviously at 2 and 6 h to the level comparable to that in the sham-operated group (P>0.05). Conclusions NO is over-expressed in the serum and spinal cord tissue in rabbits following spinal cord IR injury, and may play a role in neuronal damage and repair in the event of spinal cord IR injury.