Dabaghi S F, Kamat S G, Payne J, Marks G F, Roberts R, Schafer A I, Kleiman N S
Baylor College of Medicine, Houston, Texas 77030.
Am J Cardiol. 1994 Oct 1;74(7):720-3. doi: 10.1016/0002-9149(94)90317-4.
Aspirin interferes with platelet aggregation by inhibiting the metabolism of arachidonic acid to thromboxane A2. Although both high- and low-dose aspirin therapies are effective for secondary prophylaxis in patients with atherosclerotic vascular disease, the acute response to low-dose aspirin therapy is controversial. Eighteen volunteer subjects ingested 81, 162, or 324 mg of aspirin in a longitudinal crossover study design. Initial doses were randomly assigned and dosing intervals were separated by 2 weeks. Platelet aggregation in response to 0.9 mM arachidonic acid was measured at baseline, 15, 30, 60, and 90 minutes after ingestion. Thromboxane B2 production was assayed on simultaneously obtained samples after stimulation with arachidonic acid. The median inhibition of aggregation was 97%, 97%, and 97% 15 minutes after ingestion of 81, 162, and 324 mg, respectively. Four subjects had < 20% inhibition 15 minutes after ingesting 81 mg, but all 4 had > 90% inhibition after 30 minutes. Thromboxane B2 production declined by > 93% in all subjects at each dose. There was no difference between doses in inhibition of thromboxane B2 production.
阿司匹林通过抑制花生四烯酸代谢为血栓素A2来干扰血小板聚集。尽管高剂量和低剂量阿司匹林疗法对动脉粥样硬化性血管疾病患者的二级预防均有效,但低剂量阿司匹林疗法的急性反应仍存在争议。在一项纵向交叉研究设计中,18名志愿者受试者分别摄入81毫克、162毫克或324毫克阿司匹林。初始剂量随机分配,给药间隔为2周。在摄入阿司匹林后的基线、15分钟、30分钟、60分钟和90分钟测量对0.9毫摩尔花生四烯酸的血小板聚集情况。在用花生四烯酸刺激后,对同时采集的样本检测血栓素B2的生成。摄入81毫克、162毫克和324毫克阿司匹林后15分钟,聚集抑制中位数分别为97%、97%和97%。4名受试者在摄入81毫克后15分钟抑制率<20%,但在30分钟后均>90%。各剂量组所有受试者的血栓素B2生成均下降>93%。各剂量在抑制血栓素B2生成方面无差异。