Viinikka L, Salokannel J, Ylikorkala O
Prostaglandins Leukot Med. 1983 May;11(1):45-50. doi: 10.1016/0262-1746(83)90108-7.
We evaluated the effect of four weeks treatment with 90 mg and 1500 mg of acetylsalicylic acid (ASA), 990 mg of ASA together with 225 mg of dipyridamole and 225 mg of dipyridamole daily on the production of thromboxane A2 (TxA2) by platelets of atherosclerotic subjects. All doses of ASA studied inhibited 99% or more of TxA2 production from the third day to the end of the treatment, whereas dipyridamole did not have any effect. After the treatment, TxA2 production recovered in two weeks. Our results argue against the clinical relevance of the recent suggestions that salicylate accumulating during prolonged treatment with ASA could reduce the effect of the parent drug on the synthesis of TxA2 by platelets. Our data also dispute the inhibition of TxA2 synthesis as an antithrombotic mechanism of dipyridamole.
我们评估了每日使用90毫克和1500毫克乙酰水杨酸（ASA）、990毫克ASA联合225毫克双嘧达莫以及225毫克双嘧达莫治疗四周，对动脉粥样硬化患者血小板血栓素A2（TxA2）生成的影响。研究的所有剂量的ASA从治疗第三天到治疗结束均抑制了99%或更多的TxA2生成，而双嘧达莫没有任何作用。治疗后，TxA2生成在两周内恢复。我们的结果与近期的观点相悖，即长期使用ASA治疗期间积累的水杨酸盐会降低母体药物对血小板TxA2合成的作用，这一观点在临床上并不相关。我们的数据也对双嘧达莫抑制TxA2合成作为抗血栓形成机制提出了质疑。
