Influence of the pure synthetic PAF (platelet aggregating factor) on clot retraction and platelet aggregation.
Pure synthetic platelet aggregating factor (PAF) (1-O-Hexadecyl-2-acetyl-sn-glycero-3-phosphorylcholine) induces a dose-dependent platelet aggregation in platelet-rich plasma (PRP) and in gel-filtered platelets. Irreversible platelet aggregation was observed at final concentrations of PAF higher than 2 X 10-(7) mol/l, while reversible or two-wave aggregation was obtained with lower final concentrations. The second wave was inhibited by acetylsalicylic acid, indomethacin, dipyridamole, EDTA, EGTA, theophylline, caffeine, PGE1 and verapamil. PAF does not induce reptilase clot retraction (RCR); however, it does not inhibit RCR induced by ADP or thrombin. Since all substances known to activate platelets also induce RCR, the lack of this activity by PAF would support the existence of a third pathway in platelets.
D000818:Animals; D001790:Blood Physiological Phenomena; D003018:Clot Retraction; D003864:Depression, Chemical; D004176:Dipyridamole / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D006801:Humans; D007552:Isotonic Solutions; D008315:Malondialdehyde / Q000378:metabolism; D010972:Platelet Activating Factor / Q000502:physiology*; D010974:Platelet Aggregation / Q000187:drug effects; D051381:Rats; D014700:Verapamil / Q000494:pharmacology
D007552:Isotonic Solutions; D010972:Platelet Activating Factor; C037692:Tyrode's solution; D008315:Malondialdehyde; D004176:Dipyridamole; D014700:Verapamil