Effect of sodium arachidonate on thrombin generation through platelet activation - Inhibitory effect of aspirin

Background. Sodium arachidonate was used in this study to determine its cap acity to generate thrombin through platelet activation. Whether aspirin pre vent this effect was also investigated. Methods and Results. Seventeen heal thy volunteers without and after 160 mg/day aspirin intake for: 3-5 days we re studied. Lag-time and TG at basal condition and after platelet stimulati on 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 respective ly) 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 non-a spirinated, non-stimulated PRP and 808.9 +/- 617, in non-aspirinated PRP ac tivated with sodium arachidonate (p = 0.014). Aspirin administered red in v ivo 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 p revention of thrombosis.