| dc.description.abstract | Traumatic spinal cord injuries are often accompanied by secondary injuries that complicate the recovery process. Our lab has shown that nociceptive stimulation engages pain fibers and negatively impacts recovery following spinal cord injury (SCI). Further, nociceptive stimulation appears to increase the amount of red blood cells at the lesion site, which may indicate compromised vasculature. Progressive hemorrhagic necrosis (PHN), a phenomenon originating from the inflammatory environment induced by the initial injury, leads to the death of endothelial cells at the lesion site and hemorrhage. The present study investigated the impact of nociceptive stimulation on the amount of lesion-site hemorrhage, a hallmark of PHN. Adult rats received a laminectomy and a moderate contusion injury at the T12 vertebra. After a 24-hour recovery period, half of the subjects received noxious input in the form of electrical shock to the tail. Three hours post-shock, subjects were sacrificed and a 1-cm section of tissue around the lesion site was collected and sectioned. Following hematoxylin and eosin staining, the amount of hemorrhage was quantified as a percentage of the total section area. Subjects that received shock had more hemorrhage at and around the lesion site, compared to the unshocked group. The amount of hemorrhage peaked at the lesion epicenter and decreased with distance in both groups. Based on these findings, PHN may play a role in the detrimental effect of noxious input on recovery after SCI. Further work will examine of the effect of noxious input on capillary segmentation, another hallmark of PHN, and the cellular mechanisms that underlie these effects. | en |
