Because of the 'bland' nature of polyethylene oxide towards proteins a
nd cells, considerable effort has been devoted to preparing surfaces r
ich in polyethylene oxide, using block copolymers, surface immobilizat
ion or other methods. It is clear that these modifications result in r
educed levels of cell (including platelet) adhesion and protein adsorp
tion, when compared to unmodified and typically hydrophobic substrates
. It is far less clear whether the reduced adhesion or adsorption is d
ue specifically to the thermodynamic effects of polyethylene oxide or
to the increase in surface hydrophilicity after its immobilization. Ev
en more so, it is unclear whether the reduction in such parameters is
evidence of a reduced thrombogenicity.