Deupree J D
Epilepsia. 1977 Sep;18(3):309-15. doi: 10.1111/j.1528-1157.1977.tb04973.x.
The role or non-role of NaK ATPase, Mg ATPase, and CaMg ATPase involvement in stabilization of excitable membranes by phenytoin is critically evaluated. There is no substantial evidence to indicate that the membrane-stabilizing effect of phenytoin is due to activation of the NaK ATPase. Previous reports of activation of the NaK ATPase at low potassium and high sodium are probably not due to phenytoin but to a potassium contamination in the phenytoin solution. In vitro experiments do not provide any clear evidence of any alterations of NaK ATPase properties by phenytoin. However, one cannot rule out the possibility that phenytoin alters the efficiency of the sodium-potassium pump. Likewise, the Ca ATPase is not inhibited by phenytoin. However, there is some evidence that the Mg ATPase in synaptic vesicles is substantially inhibited by phenytoin. There is substantial evidence indicating that phenytoin partially blocks passive diffusion of sodium into stimulated nerves. The mechanism by which phenytoin blocks sodium influx and the relationship of this effect to the drug's anticonvulsant action remain to be determined.
对钠钾ATP酶、镁ATP酶和钙镁ATP酶在苯妥英稳定可兴奋膜过程中的作用或无作用进行了严格评估。没有充分证据表明苯妥英的膜稳定作用是由于钠钾ATP酶的激活。先前关于低血钾和高血钠时钠钾ATP酶被激活的报道可能并非由于苯妥英，而是由于苯妥英溶液中的钾污染。体外实验未提供苯妥英改变钠钾ATP酶特性的明确证据。然而，不能排除苯妥英改变钠钾泵效率的可能性。同样，钙ATP酶也不受苯妥英抑制。然而，有一些证据表明，突触小泡中的镁ATP酶会被苯妥英显著抑制。有充分证据表明苯妥英可部分阻断钠向受刺激神经的被动扩散。苯妥英阻断钠内流的机制以及这种作用与药物抗惊厥作用的关系仍有待确定。
