omega-Methacryloyloxyalkyl phosphorylcholine (MA-PC) polymers which have been synthesized with attention to the surface structure of a biomembrane show excellent blood compatibility, i.e., resistance to protein adsorption and blood cell adhesion. To clarify the stability of platelets in contact with the MAPC polymer surfaces, cytoplasmic free calcium concentration ([Ca2+],) in the platelets was measured. A platelet suspension was passed through a column packed with various polymer beads after treatment with plasma, and the [Ca2+]i in the platelets eluted from the column was measured. The [Ca2+]i in contact with the MAPC polymers, i.e., poly[2-methacryloyloxyethyl phosphorylcholine-co-nbutyl methacrylate (BMA)] (PMEB) and poly(6-methacryloyloxyhexyl phosphorylcholine-co-BMA) (PMHB), was less than that in contact with poly(BMA). However, poly(10-methacryloyloxydecyl phosphorylcholine-co-BMA) (PMDB) was not effective in suppressing the increase in [Ca2+]i, and thus was at the same level as in the poly(BMA). This result indicated that platelets in contact with PMEB or PMHB were less activated compared with those in contact with PMDB and poly(BMA). Moreover, the state of the platelets adhered to these polymer surfaces, both morphologically and immunologically, was examined. Scanning electron microscopic observation of the polymer surface after contact with a platelet suspension revealed that many platelets adhered and changed their shape on the poly(BMA). The numbers of adhetent platelets were reduced on all MAPC polymer surface. The relative amount of alpha-granule membrane glycoprotein (GMP-140) which appears on the cell membrane by activation of platelets on the PMEB surfaces was less than that on poly(BMA) and poly(2-hydroxyethyl methacrylate). These results suggest that PMEB and PMHB suppressed not only platelet adhesion but also activation of the platelets in contact with these surface.