Küster L J, Frölich J C
Prostaglandins. 1986 Sep;32(3):415-23. doi: 10.1016/0090-6980(86)90009-2.
The present study was undertaken in order to characterize the dose-dependent nature of acetylsalicylic acid (ASA) on platelet aggregation and plasma thromboxane B2 (TXB2) release in healthy volunteers. Volunteers received either 25, 50, 100 or 500 mg daily for five consecutive days. At the end of the five day period, all dosages of ASA were capable of completely suppressing TXB2 production and arachidonic acid-induced platelet aggregation. At that time, the second phase of ADP-induced aggregation was also blocked. However, while the inhibition following 500 mg ASA was complete after 24 hours, total inhibition with 100, 50 and 25 mg was attained only after two, three and four days, respectively, indicating the cumulative effect of ASA on platelets. Aggregation induced by collagen was also inhibited dose-dependently- yet slower and at no time complete. ASA had no inhibitory effect on aggregation by platelet-activating factor (PAF). It is concluded that a daily dose of 50 mg ASA would suffice in blocking platelet TXA2 production and aggregation induced by most physiological agents.
本研究旨在确定健康志愿者中乙酰水杨酸(ASA)对血小板聚集和血浆血栓素B2(TXB2)释放的剂量依赖性。志愿者连续五天每天分别服用25、50、100或500毫克。在五天疗程结束时,所有剂量的ASA均能完全抑制TXB2的产生以及花生四烯酸诱导的血小板聚集。此时,ADP诱导的聚集的第二阶段也被阻断。然而,虽然500毫克ASA在24小时后完全抑制,但100、50和25毫克分别在两天、三天和四天后才达到完全抑制,表明ASA对血小板有累积效应。胶原蛋白诱导的聚集也呈剂量依赖性抑制——但速度较慢且从未完全抑制。ASA对血小板活化因子(PAF)诱导的聚集没有抑制作用。得出的结论是,每日50毫克ASA足以阻断血小板TXA2的产生以及大多数生理因子诱导的聚集。