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丙戊酸钠是目前临床上应用较广的抗癫痫药，对单纯失神发作及全身强直－阵挛发作疗效最好。丙戊酸钠的抗癫痫作用机制有提高γ－氨酪酸水平及抑制神经细胞膜对Ｎａ＋的通透性等。丙戊酸钠能引起出血时间延长，这可能与影响 Von Willeband因子、减少血小板数量、降低血小板聚集及释放功能有关。血小板的数量和聚集功能可能与丙戊酸钠的剂量呈负相关。丙戊酸钠对血小板的毒性机制可能在于直接损伤造血干细胞、抑制血小板合成血栓素Ａ２及减少血小板表面活化依赖抗原。
Sodium valproate is currently widely used in clinical anti-epileptic drugs, the simple absence of seizures and generalized tonic - clonic seizures the best effect. The mechanism of antiepileptic effect of sodium valproate is to increase the level of γ-aminobutyric acid and inhibit the permeability of nerve cell membrane to Na +. Sodium valproate can cause prolonged bleeding time, which may be related to Von Willeband factor, reduce the number of platelets, reduce platelet aggregation and release function. The number and aggregation of platelets may be negatively correlated with the dose of sodium valproate. The mechanism of sodium valproate toxicity on platelets may lie in direct damage to hematopoietic stem cells, inhibition of platelet synthesis of thromboxane A2 and reduction of platelet surface activation dependent antigen.