Effect of Platelet Activating Factor(PAF) on the collagen induced platelet aggregation in whole blood.

Abstract

Studies of platelet aggregation are generally performed in p1ate1et-rich plasma(PRP) by the transmittance method. Recently, impedance aggregometry has been introduced which shows the platelet aggregability in whole blood. We compared the impedance aggregometry in whole blood with the transmittance method in PRP, with regard to collagen induced platelet aggregation. The aggregation rate in whole blood increased with increasing concentration of collagen, but remained unchanged in PRP. The factors which influence the platelet aggregation rate in whole blood were studied. CV-3988, that is the specific antagonist of PAF, acetylsalicylic acid (ASA) and phosphocreatine / creatine phosphokinase (CP/CPK) were used in order to evaluate the contribution of PAF, thromboxane and ADP in whole blood. CV-3988 dose-dependently inhibited platelet aggregation induced by collagen in whole blood, but did not inhibit the aggregation in PRP. ASA(10mM) inhibited the aggregation in whole blood incompletely too, but completely in PRP. And the inhibition of CP/CPK(CP/CPK : 1.5mM/50U/ml) was very weak in whole blood compared to that of other antagonists. The inhibitory effect of CV-3988 was investigated on the collagen induced platelet aggregation in whole blood which was pretreated with ASA ( 1 OmM ) and CP/CPK (1.5mM/50U/ml), resulting in a collagen induced aggregation in whole blood that was not completely inhibited. We conclude that there are some other different factors, which influence platelet aggregation in whole blood, in addition to thromboxane, ADP and PAF.