Karpen C W, Merola A J, Trewyn R W, Cornwell D G, Panganamala R V
Prostaglandins. 1981 Oct;22(4):651-61. doi: 10.1016/0090-6980(81)90074-5.
Platelets from vitamin E-deficient and vitamin E-supplemented rats generate the same amount of thromboxane A2 (TxA2) when they are incubated with unesterified arachidonic acid. Platelets from vitamin E-deficient rats produced more TxA2 than platelets from vitamin E-supplemented rats when the platelets are challenged with collagen. Arterial tissue from vitamin E-deficient rats generates less prostacyclin (PGI2) than arterial tissue from vitamin E- supplemented rats. The vitamin E effect with arterial tissue is observed when the tissue is incubated with and without added unesterified arachidonic acid. These data show that arterial prostacyclin synthesis is diminished in vitamin E-deficient rats. Vitamin E, in vivo, inhibits platelet aggregation both by lowering platelet TxA2 and by raising arterial PGI2.
将维生素E缺乏和补充维生素E的大鼠的血小板与未酯化的花生四烯酸一起孵育时，它们产生的血栓素A2（TxA2）量相同。当用胶原蛋白刺激血小板时，维生素E缺乏大鼠的血小板产生的TxA2比补充维生素E的大鼠的血小板更多。维生素E缺乏大鼠的动脉组织产生的前列环素（PGI2）比补充维生素E的大鼠的动脉组织少。当动脉组织在添加和不添加未酯化花生四烯酸的情况下孵育时，可观察到维生素E对动脉组织的影响。这些数据表明，维生素E缺乏的大鼠动脉前列环素合成减少。在体内，维生素E通过降低血小板TxA2和提高动脉PGI2来抑制血小板聚集。
