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Ann Thorac Surg 1994;58:1064-1068
© 1994 The Society of Thoracic Surgeons

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Articles

Inhibition of neutrophil adhesion does not prevent ischemic spinal cord injury

Division of Cardiothoracic Surgery and Department of Rehabilitation Medicine, University of Washington, Seattle, Washington, USA

Accepted for publication February 16, 1994.

^_* Address reprint requests to Dr Verrier, Division of Curdiothoracic Surgery, University of Washington, SA-25, 1959 NE Pacific St, Seattle, WA 98195.

Paraplegia may occur after transient aortic occlusion as a consequence of primary ischemia to the spinal cord or injury during the reperfusion 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 antibody (MAb 60.3) was assessed in spinal cord ischemia/reperfusion in rabbits. Spinal cord ischemia was accomplished by balloon catheter occlusion of the infrarenal aorta. Neurologic assessment was graded as normal, partial neurologic deficit, or complete paralysis. Electrophysiologic monitoring with somatosensory evoked potentials was used to determine the optimal length of time of occlusion. Animals were treated randomly 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 versus MAb, 32.4 ± 6.0 minutes). Five (55%) saline-treated and four (50%) MAb 60.3-treated animals became paraplegic. Animals with initial paraparesis all progressed to flaccid paraplegia within 24 hours. We conclude that spinal cord injury after transient aortic occlusion is independent of the [equation] glycoprotein complex of the neutrophil. Injury in this setting may occur during ischemia and thus may not be dependent on neutrophils or reperfusion.

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