Hayashi K, Fukumura H, Yamamoto N
Government Industrial Research Institute, Osaka, Japan.
J Biomed Mater Res. 1990 Oct;24(10):1385-95. doi: 10.1002/jbm.820241010.
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.
