Staiger C, Patscheke H, Neugebauer G, Kaufmann B, Strein K, Endele R, Stegmeier K
Eur J Clin Pharmacol. 1986;29(5):573-9. doi: 10.1007/BF00635895.
The pharmacokinetics and pharmacodynamic effect on platelet activation of a single 800 mg oral dose of BM 13.177 have been investigated in 8 male volunteers. BM 13.177 disappeared from plasma with a terminal elimination half-life of 0.85 h. 52% of the dose was excreted unchanged in urine. Assuming complete absorption, total clearance was calculated to be 741.3 ml/min and renal clearance to range from 310.4 to 396.9 ml/min. The pharmacodynamic studies were performed ex vivo/in vitro in studies were performed ex vivo/in vitro in platelets stimulated either with methyl mercury chloride or with U 46619. Methyl mercury chloride is a platelet activator that requires TXA2 formation from endogenous arachidonic acid, whereas U 46619 is a stable PGH2 analogue and thromboxane mimetic at the platelet TXA2/PGH2 receptor. A close correlation between the plasma concentration-time profile of BM 13.177 and inhibition of platelet shape change or aggregation was demonstrated.
在8名男性志愿者中研究了单次口服800 mg BM 13.177的药代动力学及其对血小板活化的药效学作用。BM 13.177从血浆中消除，终末消除半衰期为0.85小时。52%的剂量以原形经尿液排泄。假设完全吸收，计算得出总清除率为741.3 ml/分钟，肾脏清除率为310.4至396.9 ml/分钟。药效学研究在体外/体内进行，使用氯化甲基汞或U 46619刺激血小板。氯化甲基汞是一种血小板激活剂，需要从内源性花生四烯酸形成血栓素A2，而U 46619是一种稳定的前列腺素H2类似物，在血小板血栓素A2/前列腺素H2受体处模拟血栓素。结果表明，BM 13.177的血浆浓度-时间曲线与血小板形状改变或聚集的抑制之间存在密切相关性。
