Lagarde M, Ghazi I, Dechavanne M
Prostaglandins Med. 1979 Jun;2(6):433-9. doi: 10.1016/0161-4630(79)90127-7.
Ticlopidine, known to inhibit the primary wave of ADP-induced platelet aggregation and to increase the bleeding time, can modify platelet prostaglandin metabolism. The basal level of platelet PGE1 is enhanced by the drug. Ticlopidine does not decrease biosynthesis of prostaglandin endoperoxides from arachidonic acid but increases production of primary prostaglandins, cheifly prostaglandin D2, and causes a slight diminution of thromboxane B2 formation. The excess of prostaglandin endoperoxides not converted to primary prostglandins may escape from platelets and produce more prostacyclin if endothelial cell microsomes are present in the incubate.
噻氯匹定已知可抑制二磷酸腺苷（ADP）诱导的血小板聚集的初级波并延长出血时间，它能改变血小板前列腺素代谢。该药物可提高血小板前列腺素E1的基础水平。噻氯匹定不会降低花生四烯酸生成前列腺素内过氧化物的生物合成，但会增加主要前列腺素的生成，主要是前列腺素D2，并导致血栓素B2生成略有减少。未转化为主要前列腺素的过量前列腺素内过氧化物可能从血小板中逸出，如果孵育液中存在内皮细胞微粒体，则会产生更多前列环素。
