Taft W C, Clifton G L, Blair R E, DeLorenzo R J
Department of Neurology, Medical College of Virginia, Richmond 23298.
Brain Res. 1989 Mar 27;483(1):143-8. doi: 10.1016/0006-8993(89)90045-0.
Brief bilateral carotid occlusion in the gerbil produces forebrain ischemia that results in almost complete neuronal destruction in the CA1 sector of the hippocampus. Treatment with phenytoin (200 mg/kg) blocked the ischemia-induced neuronal death. The average density of CA1 pyramidal neurons (cells/mm CA1) was 253.6 +/- 4.4 in the sham surgery group, 12.3 +/- 3.4 in the ischemia group, and 119.5 +/- 16.6 in the group treated with phenytoin before ischemia. Thus, phenytoin reduced ischemia-produced neuronal loss in hippocampal CA1 by 44.4% (P less than 0.001). The plasma levels of phenytoin that produced this effect ranged from 28.1 to 45.0 mg per liter, with a mean phenytoin level of 34.7 +/- 1.7 mg/l (n = 10). The results suggest that phenytoin may be a clinically useful cerebroprotective agent.
沙鼠短暂双侧颈动脉闭塞会导致前脑缺血，进而致使海马体CA1区几乎完全的神经元破坏。苯妥英钠（200毫克/千克）治疗可阻止缺血诱导的神经元死亡。假手术组CA1锥体神经元的平均密度（每CA1区细胞数/毫米）为253.6±4.4，缺血组为12.3±3.4，缺血前接受苯妥英钠治疗组为119.5±16.6。因此，苯妥英钠使海马体CA1区缺血所致的神经元损失减少了44.4%（P＜0.001）。产生此效应的苯妥英钠血浆水平范围为每升28.1至45.0毫克，苯妥英钠平均水平为34.7±1.7毫克/升（n = 10）。结果表明苯妥英钠可能是一种临床上有用的脑保护剂。
