Baumel I P, Gallagher B B, Dimicco J, Dionne R
J Pharmacol Exp Ther. 1976 Jan;196(1):180-7.
The in vivo metabolism of N,N'-dimethoxymethyl phenobarbital (DMMP) and the anticonvulsant properties of its metabolites were studied in the rat. At 10 and 30 minutes after i.p. administration, DMMP (ethyl-1-14C) represented less than 3% of plasma radioactivity, whereas N-monomethoxymethyl phenobarbital (MMP) was 78 and 75%, respectively, phenobarbital (PB) 12 and 20%, apparent mephobarbital 6 and 2% and less than 5% of the radioactivity remained at the origin. Peak levels of MMP were reached at 30 minutes in liver and 60 minutes in plasma and brain. At 4 hours, MMP had declined to 7% in plasma and was not detected in brain while PB rose to 93% of total 14C in plasma and brain. SKF-525A blocked (90%) the in vivo conversion of DMMP to MMP and completely inhibited the formation of PB, apparent mephobarbital and unidentified polar metabolites. MMP after oral administration was effective against maximum electroshock seizures at a time when brain levels of PB derived from MMP were insufficient to account for the total observed protection. However, MMP appears less potent than PB against pentylenetetrazol seizures.
在大鼠体内研究了N，N'-二甲氧基甲基苯巴比妥（DMMP）的代谢及其代谢产物的抗惊厥特性。腹腔注射后10分钟和30分钟时，DMMP（乙基-1-14C）占血浆放射性的比例不到3%，而N-单甲氧基甲基苯巴比妥（MMP）分别为78%和75%，苯巴比妥（PB）为12%和20%，表观美芬妥英为6%和2%，不到5%的放射性留在原点。MMP在肝脏中的峰值水平在30分钟时达到，在血浆和脑中在60分钟时达到。4小时时，MMP在血浆中降至7%，在脑中未检测到，而PB在血浆和脑中升至总14C的93%。SKF-525A阻断了（90%）DMMP在体内向MMP的转化，并完全抑制了PB、表观美芬妥英和未鉴定的极性代谢产物的形成。口服MMP后，在源自MMP的PB脑水平不足以解释观察到的全部保护作用时，对最大电休克惊厥有效。然而，MMP对戊四氮惊厥的效力似乎低于PB。
