The hemocompatibility of a polymer containing a phospholipid polar group, poly(2-methacryloyloxyethyl phosphorylcholine (MPC)-co-n-butyl methacrylate(BMA)), with human whole blood was evaluated. When human whole blood without an anticoagulant was contacted with polymers, the blood cell adhesion and aggregation on the polymer without the MPC moiety was extensive, and considerable fibrin deposition was observed. This phenomenon was suppressed with an increase in the polymer MPC composition. Thus, the MPC moiety in the copolymer plays an important role in the nonthrombogenic behavior of the copolymer. These results were also confirmed by the whole blood coagulation time on the polymer surface which was determined by Lee-White method. The adsorption of phospholipids and proteins from human plasma on poly(MPC-co-BMA) was investigated to clarify the mechanism of the nonthrombogenicity observed with the polymer. The amount of phospholipids was increased; whereas, adsorbed proteins were decreased with an increase in the MPC composition. From these results, we concluded that the phospholipids adsorbed on poly(MPC-co-BMA) play the most important role in the nonthrombogenicity of the MPC copolymer.

Polymers with phospholipid polar groups, 2-methacryloyloxyethyl phosphorylcholine (MPC) polymers, have excellent nonthrombogenic properties. The effects of adsorption of phospholipids on platelet adhesion and activation on the MPC copolymer with n-butyl methacrylate (BMA) were investigated with particular attention to the structure of the phospholipids adsorbed onto the polymer surface. The electrical nature of the phospholipids adsorbed on the polymer surface affected the thrombogenicity of the polymer. On the MPC polymer surface treated with an aqueous liposomal solution of acidic phospholipids, phosphatidylserine, platelet adhesion and activation occurred to a greater extent when compared to a poly(MPC-co-BMA) surface. However, on the MPC polymer surface treated with electrically neutral phosphatidylcholines, reduced thrombogenicity could be observed. Therefore, the adsorption of the phosphatidylcholines was an important factor in reducing the thrombogenicity on the polymers. Moreover, by comparison of the poly(MPC-co-BMA) to a poly(BMA), platelet adhesion and activation on these polymer surfaces depended on the adsorption state of the phosphatidylcholines. The amount of phosphatidylcholine adsorbed on the poly(MPC-co-BMA) increased with an increase in the MPC mole fraction of the copolymer. This indicates that the MPC moieties have affinity for the phosphatidylcholines. We conclude that the poly(MPC-co-BMA) can adsorb large amounts of phosphatidylcholines and that these phospholipids organize themselves. The organized adsorption layer of the phosphatidylcholines on the surface, which construct biomembrane-like surfaces, can reduce platelet adhesion and activation effectively.