Journal of neurosurgery · 2002
The effect of brain temperature on hemoglobin extravasation after traumatic brain injury.
СтатьяПоддержка исследования: вне правительства СШАПоддержка службы здравоохранения СШАНазвание и аннотация: Перевод пока не подготовлен
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Kinoshita Kosaku, Chatzipanteli Katina, Alonso Ofelia F, Howard Mackenzie, Dietrich W Dalton
Аннотация
OBJECT: Although the benefits of posttraumatic hypothermia have been reported in experimental studies, the potential for therapeutic hypothermia to increase intracerebral hemorrhage remains a clinical concern. The purpose of this study was to quantify the amount of extravasated hemoglobin after traumatic brain injury (TBI) and to assess the changes in intracerebral hemoglobin concentrations under posttraumatic hypothermic and hyperthermic conditions.
METHODS: Intubated and anesthetized rats were subjected to fluid-percussion injury (FPI). In the first experiment, rats were divided into moderate (1.8-2.2 atm) and severe (2.4-2.7 atm) TBI groups. In the second experiment, the effects of 3 hours of posttraumatic hypothermia (33 or 30 degrees C), hyperthermia (39 degrees C), or normothermia (37 degrees C) on hemoglobin levels following moderate trauma were assessed. The rats were perfused with saline at 24 hours postinjury, and then the traumatized and contralateral hemispheres, including the cerebellum, were dissected from whole brain. The hemoglobin level in each brain was quantified using a spectrophotometric hemoglobin assay. The results of these assays indicate that moderate and severe FPI induce increased levels of hemoglobin in the ipsilateral hemisphere (p < 0.0001). After severe TBI, the hemoglobin concentration was also significantly increased in the contralateral hemisphere (p < 0.05) and cerebellum (p < 0.005). Posttraumatic hypothermia (30 degrees C) attenuated hemoglobin levels (p < 0.005) in the ipsilateral hemisphere, whereas hyperthermia had a marked adverse effect on the hemoglobin concentration in the contralateral hemisphere (p < 0.05) and cerebellum (p < 0.005).
CONCLUSIONS: Injury severity is an important determinant of the degree of hemoglobin extravasation after TBI. Posttraumatic hypothermia reduced hemoglobin extravasation, whereas hyperthermia increased hemoglobin levels compared with normothermia. These findings are consistent with previous data reporting that posttraumatic temperature manipulations alter the cerebrovascular and inflammatory consequences of TBI.
METHODS: Intubated and anesthetized rats were subjected to fluid-percussion injury (FPI). In the first experiment, rats were divided into moderate (1.8-2.2 atm) and severe (2.4-2.7 atm) TBI groups. In the second experiment, the effects of 3 hours of posttraumatic hypothermia (33 or 30 degrees C), hyperthermia (39 degrees C), or normothermia (37 degrees C) on hemoglobin levels following moderate trauma were assessed. The rats were perfused with saline at 24 hours postinjury, and then the traumatized and contralateral hemispheres, including the cerebellum, were dissected from whole brain. The hemoglobin level in each brain was quantified using a spectrophotometric hemoglobin assay. The results of these assays indicate that moderate and severe FPI induce increased levels of hemoglobin in the ipsilateral hemisphere (p < 0.0001). After severe TBI, the hemoglobin concentration was also significantly increased in the contralateral hemisphere (p < 0.05) and cerebellum (p < 0.005). Posttraumatic hypothermia (30 degrees C) attenuated hemoglobin levels (p < 0.005) in the ipsilateral hemisphere, whereas hyperthermia had a marked adverse effect on the hemoglobin concentration in the contralateral hemisphere (p < 0.05) and cerebellum (p < 0.005).
CONCLUSIONS: Injury severity is an important determinant of the degree of hemoglobin extravasation after TBI. Posttraumatic hypothermia reduced hemoglobin extravasation, whereas hyperthermia increased hemoglobin levels compared with normothermia. These findings are consistent with previous data reporting that posttraumatic temperature manipulations alter the cerebrovascular and inflammatory consequences of TBI.