Gordon J L, Pearson J D
Br J Pharmacol. 1978 Dec;64(4):481-3. doi: 10.1111/j.1476-5381.1978.tb17308.x.
Synthesis of prostaglandin I2, (PGI2, prostacyclin) by vascular endothelium (assayed by the ability of cultured endothelial cells to inhibit platelet aggregation) was inhibited by aspirin. At 100 mumol/l aspirin completely blocked measurable PGI2 production, but endothelial cells had substantially recovered their ability to synthesize PGI2 24 h after removal of the drug. In contrast, the effect of 1 mmol/l aspirin was still evident 24 h after drug withdrawal. Sulphinpyrazone also inhibited PGI2 synthesis, but was about 100 fold less potent than aspirin, and the effect of the drug was lost within 24 h of its addition, even when endothelial cells were left in contact with the drug during this period.
血管内皮合成前列腺素I2（PGI2，前列环素）（通过培养的内皮细胞抑制血小板聚集的能力来测定）受到阿司匹林的抑制。在100μmol/L时，阿司匹林完全阻断了可测量的PGI2生成，但在去除药物24小时后，内皮细胞已基本恢复其合成PGI2的能力。相比之下，在停药24小时后，1mmol/L阿司匹林的作用仍然明显。磺吡酮也抑制PGI2合成，但其效力比阿司匹林弱约100倍，并且在添加药物后24小时内该药物的作用就消失了，即使在此期间内皮细胞一直与药物接触。
