MacMillan V
Department of Medicine, University of Toronto, Ontario, Canada.
J Cereb Blood Flow Metab. 1988 Jun;8(3):335-40. doi: 10.1038/jcbfm.1988.68.
This study documents the effects of an intoxicating dose of ethanol on the energy metabolism and electrophysiological function of rat brain exposed for 0.5 h to ischemia produced by electrocautery of the vertebral arteries and reversible occlusion of the carotid arteries. One-hour exposure to 5 g kg-1 ethanol led to no significant alterations of the preischemic cerebral contents of glucose, lactate, or energy phosphates. Animals receiving ethanol or isovolumetric amounts of 0.9% saline showed statistically equivalent decreases in glucose, ATP, and phosphocreatine and increases in lactate, ADP, and AMP during 0.5 h of ischemia. Upon recirculation for 0.5-24 h, animals receiving ethanol again showed no significant differences from saline-treated animals in the rate of return of glucose, lactate, and energy metabolites to control levels. Animals receiving ethanol showed a trend for a faster and more complete normalization of the EEG during recirculation. It is concluded that under controlled experimental conditions, intoxicating doses of ethanol have no detrimental effect on the energy metabolism of ischemic and postischemic brain.
本研究记录了中毒剂量乙醇对大鼠脑能量代谢和电生理功能的影响，这些大鼠脑经椎动脉电烙术和颈动脉可逆性闭塞造成缺血，暴露于缺血状态0.5小时。暴露于5 g kg-1乙醇1小时未导致缺血前脑内葡萄糖、乳酸或高能磷酸化合物含量发生显著改变。在0.5小时缺血期间，接受乙醇或等体积0.9%生理盐水的动物，其葡萄糖、三磷酸腺苷（ATP）和磷酸肌酸含量在统计学上有同等程度的下降，乳酸、二磷酸腺苷（ADP）和一磷酸腺苷（AMP）含量则有同等程度的上升。再灌注0.5 - 24小时后，接受乙醇的动物在葡萄糖、乳酸和能量代谢产物恢复至对照水平的速率方面，与接受生理盐水处理的动物相比，再次显示无显著差异。接受乙醇的动物在再灌注期间脑电图有更快且更完全恢复正常的趋势。结论是，在受控实验条件下，中毒剂量的乙醇对缺血和缺血后脑的能量代谢无有害影响。
