Simrock R, Missalla A, Schwidtal P, Lischke V, Breddin H K
Thromb Haemost. 1984 Apr 30;51(2):269-71.
The results of clinical trials concerning the use of acetylsalicylic acid (ASA) as antithrombotic drug are contradictory. Inhibition by ASA of platelet prostaglandin synthesis and aggregation is prevented by its metabolite salicylic acid (SA) in animals and in human platelets in vitro. It was suggested that ASA might produce its own inhibitor, thereby diminishing its efficiency in thromboembolic disease. In four healthy male subjects there was no difference in inhibition of collagen-induced platelet aggregation after the administration of 500 mg ASA alone or at salicylate steady state (3 g SA daily). But the inhibition of tissue-extract-induced platelet shape change was diminished and shortened by pretreatment with SA. We conclude that SA does not inhibit the effects of ASA on human platelet aggregation in vivo in therapeutic dose ranges. The clinical importance of the SA/ASA-interaction on tissue-extract-induced platelet shape change remains to be clarified.
关于使用乙酰水杨酸（ASA）作为抗血栓药物的临床试验结果相互矛盾。在动物和体外人血小板中，ASA的代谢产物水杨酸（SA）可阻止其对血小板前列腺素合成和聚集的抑制作用。有人提出，ASA可能会产生自身抑制剂，从而降低其在血栓栓塞性疾病中的疗效。在四名健康男性受试者中，单独给予500mg ASA或处于水杨酸盐稳态（每日3g SA）时，对胶原诱导的血小板聚集的抑制作用没有差异。但是，SA预处理会减弱并缩短组织提取物诱导的血小板形状变化的抑制作用。我们得出结论，在治疗剂量范围内，SA不会在体内抑制ASA对人血小板聚集的作用。SA/ASA相互作用对组织提取物诱导的血小板形状变化的临床重要性仍有待阐明。
