Thomale Ulrich W, Griebenow Martin, Mautes Angelika, Beyer Thomas F, Dohse Nils-Kristian, Stroop Ralf, Sakowitz Oliver W, Unterberg Andreas W, Stover John F
Department of Neurosurgery, Charité Campus Virchow, Medical School of Berlin, Augustenburger Platz 1, D-13353 Berlin, Germany.
Neurol Res. 2007 Sep;29(6):594-603. doi: 10.1179/016164107X166272.
Following traumatic brain injury metabolic stability is impaired. Duration and reversibility of these changes might be important to guide specific interventions.
To characterize temporal and regional changes in cerebral metabolism, 68 male Sprague-Dawley rats were subjected to a focal cortical contusion. Lesion progression and mitochondrial impairment were determined by magnetic resonance imaging (MRI) and triphenyl tetrazolium chloride (TTC) staining, respectively. Metabolic alterations were determined at hours 6 and 24 and day 7 by measuring extracellular glucose, lactate and hypoxanthine levels with microdialysis catheters placed adjacent and distant to the contusion and by quantifying changes in tissue ATP, lactate and glucose using bioluminescence imaging.
The cortical lesion reached its maximal extent at hour 24 and remained confined to the ipsilateral hemisphere. In microdialysate, at hour 6, extracellular hypoxanthine and lactate reached maximal values, thereafter hypoxanthine normalized while lactate remained increased. Extracellular glucose reached the highest values at hour 24 and remained elevated. Bioluminescence imaging revealed heterogeneous changes in areas distant to the contusion. No significant changes were found in ATP content. Slightly elevated tissue glucose until 24 hours in the ipsilateral hemisphere was observed. Following a continuous increase, lactate levels were the highest by 6 hours in the ipsilateral cortex and hippocampus.
CCI is associated with disturbances in energetic metabolism. Metabolic perturbation is not restricted to the early phase and the contusional region following focal cortical contusion, but also involves hippocampus and primarily uninjured parts of the hemisphere.
创伤性脑损伤后代谢稳定性受损。这些变化的持续时间和可逆性对于指导特定干预措施可能很重要。
为了描述脑代谢的时间和区域变化，对68只雄性Sprague-Dawley大鼠进行局灶性皮质挫伤。分别通过磁共振成像（MRI）和氯化三苯基四氮唑（TTC）染色来确定损伤进展和线粒体损伤。在伤后6小时、24小时和7天，通过使用放置在挫伤附近和远处的微透析导管测量细胞外葡萄糖、乳酸和次黄嘌呤水平，并通过生物发光成像定量组织ATP、乳酸和葡萄糖的变化，来确定代谢改变。
皮质损伤在24小时达到最大范围，且局限于同侧半球。在微透析液中，伤后6小时细胞外次黄嘌呤和乳酸达到最大值，此后次黄嘌呤恢复正常而乳酸仍升高。细胞外葡萄糖在24小时达到最高值并持续升高。生物发光成像显示挫伤远处区域有不均匀变化。ATP含量未发现显著变化。观察到同侧半球在24小时内组织葡萄糖略有升高。持续升高后，同侧皮质和海马的乳酸水平在6小时时最高。
控制性皮质撞击伤与能量代谢紊乱有关。代谢紊乱不仅限于局灶性皮质挫伤后的早期阶段和挫伤区域，还涉及海马以及半球主要未受伤的部分。
