Godfrey P P, Bochner F, Grahame-Smith D G
Br J Clin Pharmacol. 1986 Oct;22(4):443-7. doi: 10.1111/j.1365-2125.1986.tb02915.x.
The effects of aspirin on the metabolism of phosphoinositides in human platelets were studied in vitro and in vivo. Eight volunteers received, at two-weekly intervals, a single dose of 10, 30, 100 or 600 mg aspirin. Before the first dose platelets were taken and incubated in vitro with a range of concentrations (10 nM-100 microM) of aspirin. Formation of inositol phosphates (IP) was measured in [3H]-inositol labelled platelets after incubation with collagen and thrombin for 30 min, a time at which a maximal increase in [3H]-IP was observed. The in vitro IC50 for inhibition of the response to collagen by aspirin was approximately 1 microM; the in vivo ID50 was 40-50 mg. Aspirin did not fully inhibit the collagen stimulated IP formation either in vitro or in vivo, and the response to thrombin was unaffected. The ID50 and IC50 of aspirin is thus in accord with the doses of aspirin associated with inhibition of platelet aggregation and thromboxane production in other studies. The possible relevance of these data to the clinical uses of aspirin is discussed.
在体外和体内研究了阿司匹林对人血小板中磷酸肌醇代谢的影响。8名志愿者每隔两周接受一次10、30、100或600毫克阿司匹林的单次剂量。在首次给药前采集血小板,并在体外与一系列浓度(10 nM - 100 μM)的阿司匹林一起孵育。在用胶原蛋白和凝血酶孵育30分钟后,在[3H] - 肌醇标记的血小板中测量肌醇磷酸(IP)的形成,在这个时间观察到[3H] - IP有最大程度的增加。阿司匹林抑制胶原蛋白反应的体外IC50约为1 μM;体内ID50为40 - 50毫克。阿司匹林在体外或体内均未完全抑制胶原蛋白刺激的IP形成,并且对凝血酶的反应未受影响。因此,阿司匹林的ID50和IC50与其他研究中与抑制血小板聚集和血栓素产生相关的阿司匹林剂量一致。讨论了这些数据与阿司匹林临床应用的可能相关性。