1. The impact of oral acetylsalicylic acid treatment on the enhancing effect of adrenaline on platelet aggregation in vitro was investigated in patients with stable angina pectoris. In addition, the influence of different anticoagulants (i.e. hirudin and citrate) on platelet aggregation in vitro was compared.

2. Eighty-four patients with stable angina pectoris were studied. Sixteen patients were on acetylsalicylic acid treatment (150-250 mg daily), whereas 68 patients were free from acetylsalicylic acid. Platelet-rich-plasma was prepared from citrate- or hirudin-antkoagulated blood. The EC50 (i.e. the concentration of agonist required to produce half-maximal aggregation) for the ADP-induced extent of aggregation was determined. Thereafter the enhancing effect of adrenaline (10 and 50 nmol/l) on ADP-induced aggregation (at EC50) was investigated.

3. In the patients with angina, acetylsalicylic acid caused the expected effects on ADP-induced platelet responses. Adrenaline significantly enhanced both the extent of aggregation and the initial rate of aggregation (primary aggregation), irrespective of the anticoagulant used. In acetylsalicylic acid-treated patients (citrated platelet-rich plasma) the extent of aggregation was partly inhibited, but no significant effect on the rate of aggregation could be observed.

4. A comparative substudy of the anticoagulants in healthy subjects (n = 8) showed that both the aggregating effect of ADP per se and the enhancing effect of adrenaline on ADP-induced aggregation (at EC50) were less influenced by acetylsalicylic acid when evaluated in hirudinized platelet-rich plasma (i.e. with physiological levels of extracellular calcium) as compared with citrated platelet-rich plasma.

5. It is concluded that acetylsalicylic acid treatment slightly attenuates the proaggregatory effect of high physiological concentrations of adrenaline in vitro. The impact of acetylsalicylic acid in vitro is, however, strongly dependent on the anticoagulant used, and is significantly weaker when evaluated in a medium with normal extracellular calcium levels (i.e. hirudin) than in a medium with low levels of extracellular calcium (citrate). Thus, acetylsalicylic acid may be a weak antagonist of catecholamine-induced platelet activation in vivo.

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