Smith C C, Wilson A P, Betteridge D J
Department of Medicine, University College London Medical School, Rayne Institute, UK.
Clin Auton Res. 1993 Feb;3(1):49-53. doi: 10.1007/BF01819144.
The aim of the study was to determine whether aspirin influences sympathoadrenal output in normal human subjects. Plasma and platelet adrenaline and noradrenaline levels were measured before and after chronic administration of oral aspirin (300 mg per day for 7 days). Catecholamine concentrations measured immediately following aspirin did not differ from control (pre-treatment) values. Platelet noradrenaline and plasma adrenaline levels were, however, significantly increased 2 weeks after cessation of treatment. Platelet TxB2 generation was significantly reduced following aspirin treatment indicating that platelet cyclooxygenase had been inhibited. Catecholamine concentrations did not correlate with TxB2 generation. In vitro platelet aggregation induced by ADP, adrenaline and collagen was reduced after aspirin providing additional confirmation of cyclooxygenase inhibition. However, the in vivo markers of platelet function, beta-TG and PF4 were unaffected. These data do not provide convincing evidence for an action of aspirin on sympathoadrenal outflow, either directly or via a prostaglandin (thromboxane) mediated effect, although this does not exclude a later, delayed effect. There was no evidence for interactions between thromboxane, catecholamine levels in plasma and platelets, and platelet function.
本研究的目的是确定阿司匹林是否会影响正常人体受试者的交感肾上腺系统输出。在口服阿司匹林（每天300毫克，持续7天）慢性给药前后，测量血浆和血小板中的肾上腺素和去甲肾上腺素水平。阿司匹林给药后立即测量的儿茶酚胺浓度与对照组（治疗前）的值没有差异。然而，在停药2周后，血小板去甲肾上腺素和血浆肾上腺素水平显著升高。阿司匹林治疗后血小板血栓素B2生成显著减少，表明血小板环氧化酶已被抑制。儿茶酚胺浓度与血栓素B2生成无关。阿司匹林后，由ADP、肾上腺素和胶原诱导的体外血小板聚集减少，进一步证实了环氧化酶受到抑制。然而，血小板功能的体内标志物β-血小板球蛋白和血小板第4因子未受影响。这些数据没有提供令人信服的证据表明阿司匹林对交感肾上腺流出有直接作用，或通过前列腺素（血栓素）介导的作用，尽管这并不排除后期延迟效应。没有证据表明血栓素、血浆和血小板中的儿茶酚胺水平与血小板功能之间存在相互作用。
