POSTTRAUMATIC HYPOTHERMIA IN THE TREATMENT OF AXONAL DAMAGE IN AN ANIMAL-MODEL OF TRAUMATIC AXONAL INJURY

Object. Many investigators have demonstrated the protective effects of hypothermia following traumatic brain injury (TBI) in both animals an d humans. Typically,:his protection has been evaluated in relation to the preservation of neurons and/or the blunting of behavioral abnormal ities. However, little consideration has been given to any potential p rotection afforded in regard to TBI-induced axonal injury, a feature o f human TBI. In this study, the authors evaluated the protective effec ts of hypothermia on axonal injury after TBT in rats. Methods. Male Sp rague-Dawley rats weighing 380 to 400 g were subjected to experimental TBI induced by an impact-acceleration device. These rats were subject ed to hypothermia either before or after injury, with their temporalis muscle and rectal temperatures maintained at 32 degrees C for 1 hour. After this I-hour period of hypothermia, rewarming to normothermic le vels was accomplished over a 90-minute period. Twenty-four hours later , the animals were killed and semiserial sagittal sections of the brai n were reacted for visualization of the amyloid precursor protein (APP ), a marker of axonal injury. The density of APP-marked damaged axons within the corticospinal tract at the pontomedullary junction was calc ulated for each animal. In all hypothermic animals, a significant redu ction in APP-marked damaged axonal density was found. In animals treat ed with preinjury, immediate postinjury, and delayed hypothermia, the density of damaged axons was dramatically reduced in comparison with t he untreated controls (p < 0.05). Conclusions. The authors infer from these findings that early as well as delayed posttraumatic hypothermia results in substantial protection in TBI, at least in terms of the in jured axons.