Thromb Haemost 2000; 84(06): 1109-1112
DOI: 10.1055/s-0037-1614178
Review Article
Schattauer GmbH

Effect of Sodium Arachidonate on Thrombin Generation through Platelet Activation – Inhibitory Effect of Aspirin

Raul Altman
2   From Centro de Trombosis de Buenos Aires, Buenos Aires, Argentina
,
Alejandra Scazziota
2   From Centro de Trombosis de Buenos Aires, Buenos Aires, Argentina
,
Jorge Rouvier
2   From Centro de Trombosis de Buenos Aires, Buenos Aires, Argentina
,
Claudio Gonzalez
1   Department of Pharmacology, School of Medicine, University of Buenos Aires, Argentina
› Author Affiliations

To Fundacion Rene Baron for supporting style correction of this paper.
Further Information

Publication History

Received 25 February 2000

Accepted after revision 07 June 2000

Publication Date:
13 December 2017 (online)

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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.