ACUTE INFLAMMATORY RESPONSE IN SPINAL-CORD FOLLOWING IMPACT INJURY

Numerous factors are involved in the spread of secondary damage in spi nal cord after traumatic injury, including ischemia, edema, increased excitatory amino acids, and oxidative damage to the tissue from reacti ve oxygen species. Neutrophils and macrophages can produce reactive ox ygen species when activated and thus may contribute to the lipid perox idation that is known to occur after spinal cord injury. This study ex amined the rostral-caudal distribution of neutrophils and macrophages/ microglia at 4, 6, 24, and 48 h after contusion injury to the T10 spin al cord of rat (10 g weight, 50 mm drop). Neutrophils were located pre dominantly in necrotic regions, with a time course that peaked at 24 h as measured with assays of myeloperoxidase activity (MPO). The sharpe st peak of MPO activity was localized between 4 mm rostral and caudal to the injury. Macrophages/microglia were visualized with antibodies a gainst ED1 and OX-42. Numerous cells with a phagocytic morphology were present by 24 h, with a higher number by 48 h. These cells were predo minantly located within the gray matter and dorsal funiculus white mat ter. The number of cells gradually declined through 6 mm rostral and c audal to the lesion. OX-42 staining also revealed reactive microglia w ith blunt processes, particularly at levels distant to the lesion. The number of macrophages/microglia was significantly correlated with the amount of tissue damage at each level. Treatments to decrease the inf lammatory response are likely to be beneficial to recovery of function after traumatic spinal cord injury. (C) 1998 Academic Press.