Zhao Q H, McNally A K, Rubin K R, Renier M, Wu Y, Rose-Caprara V, Anderson J M, Hiltner A, Urbanski P, Stokes K
Department of Macromolecular Science, Case Western Reserve University, Cleveland, Ohio 44106.
J Biomed Mater Res. 1993 Mar;27(3):379-88. doi: 10.1002/jbm.820270311.
It is hypothesized in this study that the phenomenon of environmental stress cracking (ESC) in polyetherurethane is caused by a synergistic action of biological components in the body fluids, oxidative agents, and stress. An in vitro system is designed to mimic the in vivo system; human plasma contains certain biological components that can act as a stress cracking promoter, while H2O2 (Co) solution provides an oxidative reaction comparable to that observed in the respiratory burst of adherent macrophages and foreign-body giant cells. It is demonstrated that the phenomenon of in vivo stress cracking in Pellethane 2363-80A is duplicated by an in vitro system that involves a pretreatment of prestressed specimens with human plasma at 37 degrees C for 7 days followed by oxidation in 10% hydrogen peroxide with 0.10M cobalt chloride at 50 degrees C for 10 days. The pretreatment with plasma has a synergistic effect with the oxidation by H2O2 (Co) treatment to produce ESC. A plasma component responsible for promoting stress cracking in Pellethane polyurethane is identified to be alpha 2-macroglobulin (alpha 2M).
本研究假设聚醚聚氨酯中的环境应力开裂（ESC）现象是由体液中的生物成分、氧化剂和应力的协同作用引起的。设计了一种体外系统来模拟体内系统；人血浆含有某些可作为应力开裂促进剂的生物成分，而H2O2（Co）溶液提供了与粘附巨噬细胞和异物巨细胞呼吸爆发中观察到的氧化反应相当的氧化反应。结果表明，Pellethane 2363 - 80A体内应力开裂现象可通过体外系统重现，该系统包括将预应力标本在37℃下用人血浆预处理7天，然后在50℃下于含0.10M氯化钴的10%过氧化氢中氧化10天。血浆预处理与H2O2（Co）处理的氧化作用具有协同效应，可产生ESC。已确定负责促进Pellethane聚氨酯应力开裂的血浆成分是α2 - 巨球蛋白（α2M）。
