In vivo thrombus formation induced by complement activation on polymer surfaces

To clarify involvement of complement activation in thrombus formation on polymer surfaces, in vitro complement activation was evaluated for polyethylene (PE) tubes radiation-graft copolymerized with acrylamide (AAm), acrylic acid (AC), 2-hydroxyethyl methacrylate (HEMA), N-vinylpyrrolidone (NVP), and vinyl alcohol (VOH), and compared to their in vivo antithrombogenicity and cell adherence in canine peripheral veins. The complement-activating surfaces (NVP and VOH) cause preferential adhesion of leukocytes and were more thrombogenic than the low complement-activating surfaces (AAm, PE, and HEMA). Infusion of naja haje cobra venom factor depressed leukocyte adhesion, followed by a marked decrease in thrombogenesis, for the strong classical-pathway-activating surface (NVP). Although estimation of in vitro activation for AC was inconclusive because of a large effect of adsorption, AC behaved like VOH in vivo. These results suggest that C5a(des Arg) mediated activation of leukocytes may play a role in thrombus formation by complement activation on polymer surfaces.