Toivanen J, Ylikorkala O, Viinikka L
Thromb Res. 1984 Sep 15;35(6):681-7. doi: 10.1016/0049-3848(84)90270-6.
To seek the lowest dose of acetylsalicylic acid (ASA) capable of inhibiting platelet thromboxane A2 (TxA)2 production, 18 healthy volunteers ingested 9 mg, 3 mg or 1 mg of ASA/day for twenty days and the release of TxB2 (a metabolite of TxA2) during the spontaneous clotting of blood was measured by radioimmunoassay. In addition, the production of prostacyclin (epoprostenol, PGI2) was investigated by measuring the urinary excretion of its break-down product, 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) by radioimmunoassay. Significant inhibition of platelet TxA2 production was seen from the 15th day of treatment onwards with 1 mg of ASA (maximally 15%), from the 4th day of treatment onwards with 3 mg of ASA (maximally 40%), from the 1st day of treatment onwards with 9 mg of ASA (maximally 67%). No ASA dose changed platelet counts or urinary 6-keto-PGF1 alpha excretion. One mg of ASA daily, is the lowest dose ever shown to inhibit platelet TxA2 production.
为了探寻能够抑制血小板血栓素A2(TxA)2生成的乙酰水杨酸(ASA)最低剂量,18名健康志愿者连续20天每天服用9毫克、3毫克或1毫克ASA,通过放射免疫分析法测定血液自然凝固过程中血栓素B2(TxA2的一种代谢产物)的释放量。此外,通过放射免疫分析法测量其分解产物6-酮-前列腺素F1α(6-酮-PGF1α)的尿排泄量,来研究前列环素(依前列醇,PGI2)的生成情况。从治疗第15天起,1毫克ASA可显著抑制血小板TxA2生成(最大抑制率为15%);从治疗第4天起,3毫克ASA可显著抑制(最大抑制率为40%);从治疗第1天起,9毫克ASA可显著抑制(最大抑制率为67%)。没有任何ASA剂量改变血小板计数或尿6-酮-PGF1α排泄量。每日1毫克ASA是迄今所显示的能够抑制血小板TxA2生成的最低剂量。