binge 乙醇后脑损伤和恢复：体内磁共振波谱研究证据。
Brain injury and recovery following binge ethanol: evidence from in vivo magnetic resonance spectroscopy.
机构信息
Psychiatry & Behavioral Sciences, Stanford University School of Medicine, Stanford, California 94305, USA.
出版信息
Biol Psychiatry. 2010 May 1;67(9):846-54. doi: 10.1016/j.biopsych.2009.10.028. Epub 2009 Dec 30.
BACKGROUND
The binge-drinking model in rodents using intragastric injections of ethanol (EtOH) for 4 days results in argyrophilic corticolimbic tissue classically interpreted as indicating irreversible neuronal degeneration. However, recent findings suggest that acquired argyrophilia can also identify injured neurons that have the potential to recover. The current in vivo magnetic resonance (MR) imaging and spectroscopy study was conducted to test the hypothesis that binge EtOH exposure would injure but not cause the death of neurons as previously ascertained postmortem.
METHODS
After baseline MR scanning, 11 of 19 rats received a loading dose of 5 g/kg EtOH via oral gavage, then a maximum of 3 g/kg every 8 hours for 4 days, for a total average cumulative EtOH dose of 43 +/- 1.2 g/kg and average blood alcohol levels of 258 +/- 12 mg/dL. All animals were scanned after 4 days of gavage (post-gavage scan) with EtOH (EtOH group) or dextrose (control [Con] group) and again after 7 days of abstinence from EtOH (recovery scan).
RESULTS
Tissue shrinkage at the post-gavage scan was reflected by significantly increased lateral ventricular volume in the EtOH group compared with the Con group. At the post-gavage scan, the EtOH group had lower dorsal hippocampal N-acetylaspartate and total creatine and higher choline-containing compounds than the Con group. At the recovery scan, neither ventricular volume nor metabolite levels differentiated the groups.
CONCLUSIONS
Rapid recovery of ventricular volume and metabolite levels with removal of the causative agent argues for transient rather than permanent effects of a single EtOH binge episode in rats.
背景
在啮齿动物中，通过胃内注射乙醇（EtOH）进行 4 天的狂饮模型导致嗜银皮质边缘组织，经典地解释为表明神经元不可逆转的退化。然而，最近的发现表明，获得性嗜银性也可以识别具有潜在恢复能力的受损神经元。目前的体内磁共振（MR）成像和光谱研究旨在检验以下假设，即狂饮 EtOH 暴露会造成神经元损伤，但不会像以前确定的那样导致神经元死亡。
方法
在基线 MR 扫描后，19 只大鼠中的 11 只通过口服灌胃接受 5 g/kg EtOH 的负荷剂量，然后每 8 小时最多 3 g/kg，持续 4 天，总平均累积 EtOH 剂量为 43 +/- 1.2 g/kg，平均血液酒精水平为 258 +/- 12 mg/dL。所有动物在 4 天灌胃后（灌胃后扫描）用 EtOH（EtOH 组）或葡萄糖（对照[Con]组）进行扫描，然后在戒断 EtOH 7 天后再次进行扫描（恢复扫描）。
结果
EtOH 组在灌胃后扫描时，侧脑室体积明显增大，反映出组织收缩。与 Con 组相比，EtOH 组在灌胃后扫描时背侧海马 N-乙酰天冬氨酸和总肌酸较低，胆碱含量较高。在恢复扫描时，脑室体积和代谢物水平均不能区分两组。
结论
在大鼠中，去除致病因子后，脑室体积和代谢物水平迅速恢复，这表明单次 EtOH 狂饮发作的影响是短暂的，而不是永久性的。
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