Platelet Aggregation and the Availability of Platelet Factor 3

Abstract

W e have previously shown (Hardisty and Hutton, 1965, 1966) that kaolin makes platelet factor 3 (PF 3 ) available in platelet‐rich plasma (PRP) by a reaction which involves platelet aggregation and which is inhibited by antagonisis of adenosine diphosphate (ADP), such as adenosine and related compounds. Using the kaolin clotting time system, we were not able to detect a significant effect of ADP on PRP in the absence of kaolin, and we therefore concluded that adhesion of platelets to an activating surface was also necessary for optimal effect, and that ADP aggregation alone did not make PF 3 available. This conclusion was at variance with those of Mustard, Hegardt, Rowsell and MacMillan (1964) and Castaldi, Larrieu and Caen (1965), who used different clotting systems and found evidence of increased clotting activity in platelets after ADP aggregation. We therefore decided to reinvestigate the effect of platelet aggregation on PF 3 availability, using the ‘Stypven time’ in order to eliminate the need for simultaneous activation of the earlier stages of the intrinsic coagulation process. Spaet and Cintron (1965) have already used this system to demonstrate the effect of kaolin and connective tissue on PF 3 availability.