Weksler B B, Kent J L, Rudolph D, Scherer P B, Levy D E
Stroke. 1985 Jan-Feb;16(1):5-9. doi: 10.1161/01.str.16.1.5.
We tested the antiplatelet effects of low-dose aspirin in patients with occlusive cerebrovascular disease, because conventional dosage aspirin inhibits vascular synthesis of prostacyclin at the same time that it inhibits platelets. The effects on platelet function and thromboxane A2 synthesis of 40 mg of aspirin daily or 40 mg aspirin plus dipyridamole were measured in 23 patients starting within a week after the onset of cerebral ischemia. All patients had normal baseline platelet aggregation responses to four stimuli: arachidonate, epinephrine, adenosine diphosphate and collagen. The generation of thromboxane A2 by platelets, measured as serum thromboxane B2, was also normal. After 3 to 7 days of low dose aspirin therapy, platelet aggregation responses were suppressed to the extent observed with higher dosage aspirin. Serotonin release during platelet aggregation was inhibited by more than 95% and thromboxane B2 levels in clotted blood fell by more than 95%. Responses to aspirin treatment were similar in patients with transient ischemic attacks and in those with stroke and were also similar in both sexes. No differences in platelet responses were observed between patients receiving aspirin alone and aspirin plus dipyridamole. Thus 40 mg aspirin daily inhibited platelet responses as effectively as higher doses of aspirin in patients who had recent cerebral ischemia and showed a cumulative antiplatelet effect.
我们对低剂量阿司匹林在闭塞性脑血管疾病患者中的抗血小板作用进行了测试，因为传统剂量的阿司匹林在抑制血小板的同时也会抑制血管中前列环素的合成。我们对23例在脑缺血发作后一周内开始治疗的患者，测量了每日服用40毫克阿司匹林或40毫克阿司匹林加双嘧达莫对血小板功能及血栓素A2合成的影响。所有患者对花生四烯酸、肾上腺素、二磷酸腺苷和胶原这四种刺激的血小板聚集反应基线均正常。通过测量血清血栓素B2来评估的血小板血栓素A2生成也正常。经过3至7天的低剂量阿司匹林治疗后，血小板聚集反应被抑制到与高剂量阿司匹林治疗时观察到的程度相同。血小板聚集过程中的5-羟色胺释放被抑制了95%以上，凝血血液中的血栓素B2水平下降了95%以上。短暂性脑缺血发作患者和中风患者对阿司匹林治疗的反应相似，且男女反应也相似。在单独服用阿司匹林的患者和服用阿司匹林加双嘧达莫的患者之间，未观察到血小板反应的差异。因此，对于近期发生脑缺血且显示出累积抗血小板作用的患者，每日40毫克阿司匹林抑制血小板反应的效果与高剂量阿司匹林一样有效。
