Early and sustained alterations in cerebral metabolism after traumatic brain injury in immature rats
Early and sustained alterations in cerebral metabolism after traumatic brain injury in immature rats
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DOI：
10.1089/neu.2007.0481
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发表时间：
2008-06-01
影响因子：
4.2
通讯作者：
Robertson, Courtney L.
中科院分区：
文献类型：
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作者：
Casey, Paula A.;Mckenna, Mary C.;Robertson, Courtney L.
虽然研究表明创伤性脑损伤(TBI)后大脑代谢发生了变化，但有关发育中脑的临床数据有限。我们假设创伤后代谢变化发生在早期(24小时)，并持续长达一周。幼年大鼠左侧顶叶皮质行颅脑损伤。分别于伤后4小时、24小时和7天取脑，分成同侧(损伤侧)和对侧(对照)半球。获得了N-乙酰-天冬氨酸(NAA)、乳酸(Lac)、肌酸(Cr)、胆碱和丙氨酸的核磁共振波谱，并测定了代谢物的比值(NAA/Cr、Lac/Cr)。在假对照组中，大脑半球之间的代谢在任何时候都没有差异。在4小时和24小时，Lac/Cr升高，反映糖酵解增加和/或氧化代谢降低。伤后24小时和7天，NAA/Cr下降，提示神经元完整性受损。大鼠脑损伤后4小时、24小时、7天，NAA/Lac比值均降低(接近15-20%)。总而言之，未成熟大鼠在脑损伤后早期(24小时)就开始代谢紊乱，并可持续7天。对脑外伤后早期代谢变化的评估可以确定发育中大脑神经保护的新靶点。
Although studies have shown alterations in cerebral metabolism after traumatic brain injury (TBI), clinical data in the developing brain is limited. We hypothesized that post-traumatic metabolic changes occur early (< 24 h) and persist for up to 1 week. Immature rats underwent TBI to the left parietal cortex. Brains were removed at 4 h, 24 h, and 7 days after injury, and separated into ipsilateral (injured) and contralateral (control) hemispheres. Proton nuclear magnetic resonance (NMR) spectra were obtained, and spectra were analyzed for N-acetyl-aspartate (NAA), lactate (Lac), creatine (Cr), choline, and alanine, with metabolite ratios determined (NAA/Cr, Lac/Cr). There were no metabolic differences at any time in sham controls between cerebral hemispheres. At 4 and 24 h, there was an increase in Lac/Cr, reflecting increased glycolysis and/or decreased oxidative metabolism. At 24 h and 7 days, there was a decrease in NAA/Cr, indicating loss of neuronal integrity. The NAA/Lac ratio was decreased (similar to 15-20%) at all times (4 h, 24 h, 7 days) in the injured hemisphere of TBI rats. In conclusion, metabolic derangements begin early (< 24 h) after TBI in the immature rat and are sustained for up to 7 days. Evaluation of early metabolic alterations after TBI could identify novel targets for neuroprotection in the developing brain.