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Departments of *Neurology,
Anesthesiology, and
Physiology, College of Medicine, University of South Florida, Tampa, Florida; and
Oncology Program, H. Lee Moffitt Cancer Center, University of South Florida, Tampa, Florida
Address correspondence and reprint requests to Kamatham A. Naidu, PhD, Sammons Tower, Ste. 4802, 3535 Worth St., Dallas, TX 75246. Address e-mail to KamathaN{at}Baylorhealth.edu
The pathophysiology of ischemia/reperfusion injury involves extravascular migration of leukocytes from the bloodstream to the site of injury. Leukocyte adhesion and intercellular adhesion molecule-1 (ICAM-1) play an important role in the recruitment of leukocytes to the site of injury. In this study, we evaluated the role of the ICAM-1 in spinal cord ischemia and the therapeutic effects of epidural ICAM-1 monoclonal antibody (Mab). The descending aorta was occluded below the renal artery with an aneurysm clip in rabbits anesthetized with halothane. The following variables were evaluated, in addition to ICAM-1 expression in the lumbar spinal cord, in animals receiving saline or ICAM-1 Mab via the epidural route: (1) leukocyte recruitment in the lumen of capillary vessels of the lumbar spinal cord (L6-7) at 8 h after 30 min of aortic occlusion and (2) neurological evaluation at 20 h after aortic occlusion of 10, 15, 17.5, 20, or 25 min. Paraplegia was graded with the following scale: Grade 0, no deficit; Grade 1, partial deficit; and Grade 2, complete paraplegia. Spinal cord ischemia increased the expression of ICAM-1 in the endothelium of spinal cord capillaries and led to capillary leukocyte recruitment and extravascular migration into the lumbar spinal cord parenchyma, which was ablated with epidural ICAM-1 Mab. Epidural ICAM-1 Mab reduced neurological deficits and offered neuroprotection. These findings demonstrate the involvement of the ICAM-1 pathway in spinal cord ischemia and the neuroprotective effects of epidural ICAM-1 Mab. Strategies to ameliorate spinal cord ischemia may entail the administration of leukocyte antiadhesion molecules into the neuraxial space.
IMPLICATIONS: Spinal cord ischemia increased intercellular adhesion molecule-1 (ICAM-1) expression and leukocyte recruitment. Epidural administration of ICAM-1 monoclonal antibody ablated leukocyte recruitment and reduced neurological deficits.
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  I. K. Toumpoulis, J. C. Papakostas, M. I. Matsagas, V. D. Malamou-Mitsi, L. S. Pappa, G. E. Drossos, J. J. DeRose, and C. E. Anagnostopoulos Superiority of early relative to late ischemic preconditioning in spinal cord protection after descending thoracic aortic occlusion J. Thorac. Cardiovasc. Surg., November 1, 2004; 128(5): 724 - 730. [Abstract] [Full Text] [PDF]
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