Dienel A, Andreas K, Schmidt J
Biomed Biochim Acta. 1984;43(10):1179-84.
We used the effect of ethanol on the convulsion threshold as model of injuriousness to analyse the CNS protective efficacy of nootropics. The CD50 of picrotoxine in mice was significantly diminished in comparision with the controls between 5 and 6 hours after 66 mmol/kg ethanol administered intraperitoneally and between 7 and 8 h after 92.4 mmol/kg. In this moment the administered ethanol was already eliminated; the effect is explained as a reversible consequence of the previous ethanol exposition. The influence of nootropics was examined. Piracetam (0.7 mmol/kg i.p.) as well as methylglucaminorotate (MGO) (0.68 mmol/kg-1 i.p.) suppressed the ethanol effect on the convulsibility, pyritinol (0.82 mmol/kg) was ineffective, and meclophenoxate (1.02 mmol/kg) by itself decreased the convulsions threshold.
我们以乙醇对惊厥阈值的影响作为伤害性模型,来分析促智药对中枢神经系统的保护功效。与对照组相比,腹腔注射66 mmol/kg乙醇后5至6小时以及注射92.4 mmol/kg乙醇后7至8小时,小鼠中苦味毒的半数惊厥剂量(CD50)显著降低。此时,所注射的乙醇已被清除;这种效应被解释为先前乙醇暴露的可逆后果。我们研究了促智药的影响。吡拉西坦(0.7 mmol/kg腹腔注射)以及甲葡胺半胱氨酸(MGO)(0.68 mmol/kg腹腔注射)可抑制乙醇对惊厥性的影响,吡硫醇(0.82 mmol/kg)无效,而甲氯芬酯(1.02 mmol/kg)本身会降低惊厥阈值。