Posttraumatic hypothermia reduces polymorphonuclear leukocyte accumulation following spinal cord injury in rats

The present study addresses the effects of moderate posttraumatic hypothermia (32°C) on the temporal and regional profile of polymorphonuclear leukocyte (PMNL) accumulation after traumatic spinal cord injury (SCI). We hypothesized that posttraumatic hypothermia would reduce the degree of inflammation by reducing PMNL infiltration. Rats underwent moderate spinal cord injury at T10 using the NYU impactor device. In the first study, the temporal profile of myeloperoxidase (MPO) activity (a marker of neutrophil accumulation) under normothermic (37°C) conditions was determined. The animals were allowed to survive for 3 or 24 h, or 3 or 7 days after SCI. Spinal cords were dissected into five segments rostral and caudal to the injury site. Additional animals were studied for the immunocytochemical visualization of MPO. In the second study, rats were sacrificed at 24 h after a monitoring period of normothermia (36.5°C/3 h) or hypothermia (32.4°C/3 h) with their controls. In the time course studies, MPO enzymatic activity was significantly increased at 3 and 24 h within the traumatized T10 segment compared to controls. MPO activity was also increased at 3 h within the rostral T8 and T9 segments and caudal T11 and T12 segments compared to controls. At 24 h after trauma, MPO activity remained elevated within both the rostral and caudal segments compared to control. By 3 days, the levels of MPO activity were reduced compared to the 24-h values but remained significantly different from control. Neutrophils that exhibited MPO immunoreactivity were seen at 6 and 24 h, with a higher number at 3 days. PMNLs were located within the white and gray matter of the lesion and both rostral and caudal to the injury site. Posttraumatic hypothermia reduced MPO activity at 24 h in the injured spinal cord segment, compared to normothermic values. The results of this study indicate that a potential mechanism by which hypothermia improves outcome following SCI is by attenuating posttraumatic inflammation.