INHIBITION OF NEUTROPHIL ADHESION DOES NOT PREVENT ISCHEMIC SPINAL-CORD INJURY

Paraplegia may occur after transient aortic occlusion as a consequence of primary ischemia to the spinal cord or injury during the reperfusi on period. In animal models of ischemia/reperfusion there is evidence that reperfusion injury may be modulated partially by neutrophils. The efficacy of the neutrophil adherence blocking murine monoclonal antib ody (MAb 60.3) was assessed in spinal cord ischemia/reperfusion in rab bits. Spinal cord ischemia was accomplished by balloon cathetel occlus ion of the infrarenal aorta. Neurologic assessment was graded as norma l, partial neurologic deficit, or complete paralysis. Electrophysiolog ic monitoring with somatosensory evoked potentials was used to determi ne the optimal length of time of occlusion. Animals were treated rando mly with 2 mg/kg of intravenous MAb 60.3 (n = 8) or saline solution (n = 9) with the investigator unaware of treatment. Mean occlusion times were no different between groups (control, 32.7 +/- 3.6 minutes versu s MAb, 32.4 +/- 6.0 minutes). Five (55%) saline-treated and four (50%) MAb 60.3-treated animals became paraplegic. Animals with initial para paresis all progressed to flaccid paraplegia within 24 hours. We concl ude that spinal cord injury after transient aortic occlusion is indepe ndent of the CD11/CD18 glycoprotein complex of the neutrophil. Injury in this setting may occur during ischemia and thus may not be dependen t on neutrophils or reperfusion.