Summary
Background. Sodium arachidonate was used in this study to determine its capacity to generate thrombin through platelet activation. Whether aspirin prevent this effect was also investigated. Methods and Results. Seventeen healthy volunteers without and after 160 mg/day aspirin intake for 3-5 days were studied. Lag-time and TG at basal condition and after platelet stimulation by sodium arachidonate (AA) were measured in normal non-aspirinated as well as “in vivo” aspirinated platelet rich plasma. (PRP). The lag-time was statistically significant shorter in non-aspirinated PRP activated with AA compared with non-activated PRP. This effect was inhibited by aspirin. In non-aspirinated PRP, there was an increase of TG at 4 and 6 min. incubation when platelets were activated with AA but the difference disappeared after 8 min. incubation, (84 ± 71; 148 ± 58 and 142 ± 92 nmol/L respectively) compared with non-aspirinated, non-activated platelets (16 ± 23; 55 ± 56 and 111 ± 76 nmol/L at 4, 6 and 8 min, p < 0.0001, p < 0.0001 and p = 0.292, respectively). The AUCo→22 min were 520.6 ± 545.5 in nonaspirinated, non-stimulated PRP and 808.9 ± 617, in non-aspirinated PRP activated with sodium arachidonate (p = 0.014). Aspirin administered in vivo produced a decrease of TG in PRP activated with AA.
Conclusion. Platelet activated by AA trigged TG. This effect was inhibited by aspirin and could be an additional beneficial effect of aspirin in the prevention of thrombosis.
Key words
Aspirin - platelet aggregation inhibitors - thrombin generation.
