Park K D, Suzuki K, Lee W K, Lee J E, Kim Y H, Sakurai Y, Okano T
Polymer Chemistry Lab., Korea Institute of Science and Technology, Seoul, Korea.
ASAIO J. 1996 Sep-Oct;42(5):M876-81. doi: 10.1097/00002480-199609000-00117.
Polyurethane (PU) surfaces were modified by coupling polyethylene glycol (PEG; molecular weight, 1,000) chains carrying different terminal groups (PU-PEG1K-OH, PU-PEG1K-NH2, PU-PEG1K-SO3) and longer PEG chains (MW, 3,350; PU-PEG3.4K-OH). The modified PU surfaces have the same PEG (1K) chain density. Surface induced platelet activation was evaluated by measuring cytoplasmic free calcium concentration in platelets contacting modified surfaces, and platelet adhesion onto modified surfaces was investigated in vitro. Cytoplasmic free calcium levels in platelets contacting PU-PEG-SO3 remained relatively constant, in contrast to the significant increase observed for PU-PEG-NH2, PU-PEG-OH, and control PU surfaces. The degree of platelet adhesion clearly demonstrates that all PEG graft surfaces prevented platelet adhesion. Among PEG1K surfaces, PU-PEG-SO3 shows the lowest platelet adhesion. In the case of relatively longer PEG grafted surfaces (PU-PEG3.4K-OH and PU-PEG3.4K-Hep), both surfaces were found to prevent the increase in both cytoplasmic free calcium and platelet adhesion. These results suggest that longer PEG chain grafting is more effective than shorter grafting in preventing platelet activation and adhesion because of the highly dynamic movement of hydrated PEG chains at the interface. In addition, in vitro platelet interaction is dependent upon terminal groups of PEG chains on PEG1K series surfaces.
通过连接带有不同端基（PU-PEG1K-OH、PU-PEG1K-NH2、PU-PEG1K-SO3）的聚乙二醇（PEG；分子量为1000）链以及更长的PEG链（分子量3350；PU-PEG3.4K-OH）对聚氨酯（PU）表面进行改性。改性后的PU表面具有相同的PEG（1K）链密度。通过测量与改性表面接触的血小板中的细胞质游离钙浓度来评估表面诱导的血小板活化，并在体外研究血小板在改性表面上的黏附情况。与PU-PEG-NH2、PU-PEG-OH和对照PU表面观察到的显著增加相比，与PU-PEG-SO3接触的血小板中的细胞质游离钙水平保持相对恒定。血小板黏附程度清楚地表明，所有PEG接枝表面都能防止血小板黏附。在PEG1K表面中，PU-PEG-SO3的血小板黏附率最低。在相对较长的PEG接枝表面（PU-PEG3.4K-OH和PU-PEG3.4K-Hep）的情况下，发现这两种表面都能防止细胞质游离钙增加和血小板黏附。这些结果表明，由于水合PEG链在界面处的高度动态运动，较长的PEG链接枝在防止血小板活化和黏附方面比较短的接枝更有效。此外，体外血小板相互作用取决于PEG1K系列表面上PEG链的端基。
