[The effects of platelet-activating factor (PAF) on the collagen-induced whole blood aggregation].

: The role of platelet-activating factor (PAF) on collagen-induced whole blood aggregation was studied. First, the collagen-induced whole blood aggregation was examined using impedance aggregometry. Even if whole blood was pretreated with both acetylsalicylic acid (aspirin, ASA) and CP/CPK (creatine phosphate and creatine phosphokinase) to inhibit arachidonic acid metabolites products in the cyclooxygenase pathway and ADP, whole blood aggregation was induced by collagen in a concentration-dependent manner. This suggest that other factors, including PAF, led to this aggregation. Even though addition of CV3988 (specific PAF inhibitor) with ASA and CP/CPK had no further effect on collagen-induced whole blood aggregation, collagen-induced whole blood aggregation was significantly reduced in whole blood pretreated with CV3988 or ASA alone; but not with CP/CPK alone. Next, synthesized PAF from washed platelets or washed leukocytes stimulated with collagen or ONO-11113 (STA2; stable analogue of thromboxane A2), and the inhibiting effects of ASA on the PAF synthesis from collagen-stimulated leukocytes were examined, using a radioimmunoassay kit for PAF. Collagen stimulated the leukocytes PAF synthesis but not the platelets PAF synthesis. STA2 also stimulated leukocytes PAF synthesis. ASA pretreatment of leukocytes significantly reduced the collagen-induced PAF synthesis. Thus, PAF seemed to affect collagen-induced whole blood aggregation and ASA seemed to inhibit PAF synthesis. From these results, I conclude PAF (synthesized from leukocytes directly stimulated with collagen or indirectly with thromboxane A2 from collagen-stimulated platelets) plays an important role in collagen-induced whole blood aggregation.