The effect of ethanol on human brain metabolites longitudinally characterized by proton MR spectroscopy
The effect of ethanol on human brain metabolites longitudinally characterized by proton MR spectroscopy
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DOI：
10.1038/jcbfm.2009.12
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发表时间：
2009-05-01
影响因子：
6.3
通讯作者：
Bendszus, Martin
中科院分区：
文献类型：
--
作者：
Biller, Armin;Bartsch, Andreas J.;Bendszus, Martin
乙醇对人脑的影响尚未通过纵向磁共振（MR）光谱实验来解决。因此，我们通过质子磁共振光谱（（1）H-MRS）纵向表征了15名健康个体摄入标准饮料后的大脑代谢物变化（平均血液酒精峰值浓度（BAC）：51.43 +/- 10.27 mg/dL）。每名参与者在口服酒精暴露前、暴露后93.71 +/- 11.17分钟和暴露后726.36 +/- 94.96分钟（12.11 +/- 1.58小时）进行了检查。通过光谱数据的LC模型分析确定，额中和小脑乙醇浓度随时间的变化相似。酒精诱导的额内侧肌酸、胆碱、葡萄糖、肌醇和天冬氨酸水平的变化在摄入后持续5.79 +/- 2.94分钟，以及暴露后小脑胆碱和肌醇水平持续8.64 +/- 2.98分钟。与乙醇浓度密切相关，幕上肌酸，胆碱，肌醇和天冬氨酸水平降低乙醇给药后，而葡萄糖水平增加。同样，幕下胆碱和肌醇浓度与乙醇水平随时间呈负相关。酒精暴露后，N-乙酰天冬氨酸水平没有变化。此外，未检测到乙醇对脑水积分的影响。乙醇的消耗可能会直接增加氧化应激和神经元的脆弱性it. Alternatively，我们的研究结果是兼容的乙醇诱导的细胞膜修饰和替代能源基板使用酒精暴露后。Journal of Cerebral Blood Flow & Metabolism（2009）29，891-902; doi：10.1038/jcbfm.2009.12; 2009年2月25日在线发表
The effect ethanol exerts on the human brain has not yet been addressed by longitudinal magnetic resonance (MR) spectroscopic experiments. Therefore, we longitudinally characterized cerebral metabolite changes in 15 healthy individuals by proton magnetic resonance spectroscopy ((1)H-MRS) subsequent to the ingestion of a standard beverage (mean peak blood alcohol concentration (BAC): 51.43 +/- 10.27 mg/dL). Each participant was examined before, over 93.71 +/- 11.17 mins immediately after and 726.36 +/- 94.96 mins (12.11 +/- 1.58 h) past per os alcohol exposure. Fronto-mesial and cerebellar ethanol concentrations over time were similar as determined by the LCModel analysis of spectral data. Alcohol-induced changes of fronto-mesial creatine, choline, glucose, inositol and aspartate levels for 5.79 +/- 2.94 mins upon ingestion as well as cerebellar choline and inositol levels for 8.64 +/- 2.98 mins past exposure. Closely associated with ethanol concentrations, supratentorial creatine, choline, inositol and aspartate levels decreased after ethanol administration, whereas glucose levels increased. Similarly, infratentorial choline and inositol concentrations were negatively correlated with ethanol levels over time. There were no changes in N-acetyl-aspartate levels upon alcohol exposure. Furthermore, no influence of ethanol on brain water integrals was detected. Ethanol consumption may directly increase oxidative stress and the neuronal vulnerability to it. In addition, our results are compatible with ethanol-induced cell membrane modifications and alternative energy substrate usage upon alcohol exposure. Journal of Cerebral Blood Flow & Metabolism (2009) 29, 891-902; doi:10.1038/jcbfm.2009.12; published online 25 February 2009