COMPLEMENT-MEDIATED LEUKOCYTE ADHESION ON POLY(ETHERURETHANE UREAS) UNDER SHEAR-STRESS IN-VITRO

Blood-contacting biomaterials may activate the complement cascade, thu s promoting leukocyte adhesion to the biomaterial surface. We hypothes ize that the extent of complement activation is modulated by biomateri al formulation and the presence of fluid shear stress. To investigate this hypothesis, we tested base poly(etherurethane ureas) formulated w ith or without Santowhite(R) antioxidant, a nucleophilic additive. We found that adherent leukocyte densities decreased with increasing shea r stress. Moreover, leukocyte adhesion was decreased significantly fur ther by Santowhite(R) additive under shear stress but not under static conditions. Monocytes showed a higher propensity for adhesion than di d neutrophils under shear and static conditions. Under static conditio ns, adherent cells on the Santowhite(R)-containing polyurethane had a slightly more activated morphology than those on the base polyurethane . Cell adhesion under shear stress was significantly decreased when C3 or fibronectin was depleted from the suspension medium. Santowhite(R) additive increased Factor B adsorption to the test surface while shea r stress increased Factor H adsorption. The combination of Santowhite( R) additive and shear stress increased the adsorption of both Factor B and Factor H and the serum protein S-terminal complement complex leve ls, but it did not further increase the state of activation of adheren t cells. We conclude the leukocyte adhesion on poly(etherurethane urea ) surfaces is sensitive to the levels of shear stress and that both C3 and fibronectin are required to maintain adhesion in the presence of shear stress. The low state of cellular activation and increased Facto r H adsorption may explain the decreased adherent leukocyte density on the Santowhite(R)-containing polyurethane. (C) 1996 John Wiley & Sons , Inc.