The influence of inflammatory mediators on the pathophysiology of delayed paraplegia after spinal cord ischemia.

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Recently, high mobility group box 1 protein (HMGB1) related to cytokine gets into the limelight. We investigated whether the ischemic spinal cord injury in rabbits was reduced to inhibit the activation of HMGB1. We assigned rabbits to three groups (n=5 in each); a control group, low dose anti- HMGB1 antibody group (segmental administration of 1000μg anti- HMGB1 antibody), high dose anti- HMGB1 antibody group (segmental administration of 2000μg anti- HMGB1 antibody). Spinal cord ischemia was produced by occluding the abdominal aorta for 13 min. After the reperfusion, hindlimb motor function (score range: 4, normal to 0, paraplegia) was assessed daily for 7 days, and then the number of normal neurons in the anterior spinal cord was counted. There were no significant intergroup differences in neurological scores and the numbers of normal neurons. The ischemic spinal cord injury in rabbits was not reduced to inhibit the activation of HMGB1.