van Gijn J
University Department of Neurology, University Hospital, Utrecht, The Netherlands.
Neurol Clin. 1992 Feb;10(1):193-207; discussion 208.
Until recently, a gap existed between the rapidly advancing knowledge about the pharmacology of aspirin and the management of patients who are threatened by stroke. In doses as low as 20 to 40 mg per day, aspirin can completely suppress the production of the aggregant agent thromboxane A2. The clinical evidence, however, which shows a reduction of 20% to 25% in the incidence of vascular death, stroke, or myocardial infarction, is based on trials with 300 to 1300 mg of aspirin per day. The clinicians are catching up now that recent trials have demonstrated similar effects with 30 or 75 mg of aspirin per day, and with fewer side effects. The hope that the protective effects of these low doses would be even greater, thanks to the sparing of the prostaglandin synthesis in endothelial tissue, has not yet materialized.
直到最近，在阿司匹林药理学方面迅速增长的知识与受中风威胁患者的治疗之间仍存在差距。每天低至20至40毫克的剂量，阿司匹林就能完全抑制聚集剂血栓素A2的产生。然而，临床证据显示血管性死亡、中风或心肌梗死的发生率降低了20%至25%，这些证据是基于每天服用300至1300毫克阿司匹林的试验得出的。由于最近的试验表明，每天服用30或75毫克阿司匹林也有类似效果，且副作用更少，临床医生现在正在迎头赶上。由于内皮组织中前列腺素合成得以保留，人们曾希望这些低剂量的保护作用会更大，但这一希望尚未实现。
