H Koizumi1, J T Povlishock. 1. Department of Anatomy, Medical College of Virginia, Virginia Commonwealth University, Richmond 23298-0709, USA.
Abstract
OBJECT: Many investigators have demonstrated the protective effects of hypothermia following traumatic brain injury (TBI) in both animals and humans. Typically, this protection has been evaluated in relation to the preservation of neurons and/or the blunting of behavioral abnormalities. However, little consideration has been given to any potential protection afforded in regard to TBI-induced axonal injury, a feature of human TBI. In this study, the authors evaluated the protective effects of hypothermia on axonal injury after TBI in rats. METHODS: Male Sprague-Dawley rats weighing 380 to 400 g were subjected to experimental TBI induced by an impact-acceleration device. These rats were subjected to hypothermia either before or after injury, with their temporalis muscle and rectal temperatures maintained at 32 degrees C for 1 hour. After this 1-hour period of hypothermia, rewarming to normothermic levels was accomplished over a 90-minute period. Twenty-four hours later, the animals were killed and semiserial sagittal sections of the brain 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 calculated for each animal. In all hypothermic animals, a significant reduction in APP-marked damaged axonal density was found. In animals treated with preinjury, immediate postinjury, and delayed hypothermia, the density of damaged axons was dramatically reduced in comparison with the untreated controls (p < 0.05). CONCLUSION: 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 injured axons.
OBJECT: Many investigators have demonstrated the protective effects of hypothermia following traumatic brain injury (TBI) in both animals and humans. Typically, this protection has been evaluated in relation to the preservation of neurons and/or the blunting of behavioral abnormalities. However, little consideration has been given to any potential protection afforded in regard to TBI-induced axonal injury, a feature of human TBI. In this study, the authors evaluated the protective effects of hypothermia on axonal injury after TBI in rats. METHODS: Male Sprague-Dawley rats weighing 380 to 400 g were subjected to experimental TBI induced by an impact-acceleration device. These rats were subjected to hypothermia either before or after injury, with their temporalis muscle and rectal temperatures maintained at 32 degrees C for 1 hour. After this 1-hour period of hypothermia, rewarming to normothermic levels was accomplished over a 90-minute period. Twenty-four hours later, the animals were killed and semiserial sagittal sections of the brain 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 calculated for each animal. In all hypothermic animals, a significant reduction in APP-marked damaged axonal density was found. In animals treated with preinjury, immediate postinjury, and delayed hypothermia, the density of damaged axons was dramatically reduced in comparison with the untreated controls (p < 0.05). CONCLUSION: 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 injured axons.
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