Abstract
ARACHIDONIC acid (AA) is converted into prostaglandins (PG) E2 and F2α by PG synthetase contained in mammalian tissues1,2. A material showing vasocontracting activity and called rabbit aorta contracting substance (RCS)3 has been suggested to be the cyclic endoperoxide intermediate formed during the biosynthesis of these prostaglandins4,5. The participation of RCS in inflammation has been proposed as its biosynthesis, like that of PG, is inhibited by anti-inflammatory drugs (AID)5–7. Platelets synthesize PG when reacted with collagen or thrombin8,9 or directly with AA10. Collagen-induced platelet aggregation is inhibited by AID11 and contact with collagen by damaged vessels is believed to be the initial stimulus for platelet aggregation in vivo12. No connexion has been proposed as yet between platelet aggregation, synthesis of PG and their common inhibition by AID. We have now demonstrated that AA induces platelet aggregation with generation of RCS and PG. As both responses were hindered by AID, it is suggested that PG synthetase interferes with platelet function other than through PG. An intermediate such as RCS may play the central role. Human or rabbit platelet rich plasma (hPRP or rPRP) and other blood elements were obtained as indicated in Fig. 1 and aggregation was studied turbidimetrically13 at room temperature.
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VARGAFTIG, B., ZIRINIS, P. Platelet Aggregation induced by Arachidonic Acid is accompanied by Release of Potential Inflammatory Mediators distinct from PGE2 and PGF2. Nature New Biology 244, 114–116 (1973). https://doi.org/10.1038/newbio244114a0
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DOI: https://doi.org/10.1038/newbio244114a0
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