Tsien W H, Sass S P, Sheppard H
Thromb Res. 1982 Nov 15;28(4):509-19. doi: 10.1016/0049-3848(82)90167-0.
Arachidonic acid (AA) induced aggregation of canine platelets can be inhibited by various phosphodiesterase inhibitors (PDIs) with the order of potency IBMX greater than or equal to papaverine greater than Ro 20-1724 greater than theophylline. With aggregation induced by AA plus epinephrine (EPI), only IBMX and papaverine inhibited at 100 microM. None of these PDIs affected the basal cAMP levels but all potentiated the PGE1-stimulated cAMP production, with the order of potency being Ro 20-1724 greater than papaverine greater than IBMX greater than theophylline. PGE1 at 1 microM caused a sharp increase in cAMP and complete inhibition of platelet aggregation induced by AA plus EPI. However, when EPI was added before PGE1, there was no elevation of cAMP yet inhibition of aggregation still occurred. Our results indicated that inhibition of platelet aggregation does not require a measurable increase in cAMP.
花生四烯酸（AA）诱导的犬血小板聚集可被多种磷酸二酯酶抑制剂（PDIs）抑制，其效力顺序为异丁基甲基黄嘌呤（IBMX）≥罂粟碱＞Ro 20-1724＞茶碱。对于由AA加肾上腺素（EPI）诱导的聚集，仅IBMX和罂粟碱在100微摩尔时具有抑制作用。这些PDIs均不影响基础环磷酸腺苷（cAMP）水平，但均增强了前列腺素E1（PGE1）刺激的cAMP生成，其效力顺序为Ro 20-1724＞罂粟碱＞IBMX＞茶碱。1微摩尔的PGE1导致cAMP急剧增加，并完全抑制由AA加EPI诱导的血小板聚集。然而，当在PGE1之前加入EPI时，cAMP没有升高，但聚集仍被抑制。我们的结果表明，抑制血小板聚集并不需要cAMP有可测量的增加。
