Max Bergmann Center of Biomaterials Dresden, Leibniz Institute of Polymer Research Dresden, Dresden, Germany.
J Mater Sci Mater Med. 2010 Mar;21(3):931-7. doi: 10.1007/s10856-009-3912-0. Epub 2009 Oct 23.
Biomaterial induced coagulation encompasses plasmatic and cellular processes. The functional loss of biomedical devices possibly resulting from these thrombotic reactions motivates the need for a better understanding of processes occurring at blood-biomaterial interfaces. Well defined model surfaces providing specific chemical-physical properties (self assembled monolayers (SAMs)) displaying hydrophobic or/and acidic terminal groups were used to uncover initial mechanisms of biomaterial induced coagulation. We investigated the influence of electrical charge and wettability on platelet- and contact activation, the two main actors of blood coagulation, which are often considered as separate mechanisms in biomaterials research. Our results show a dependence of contact activation on acidic surface groups and a correlation of platelet adhesion to surface hydrophobicity. Clot formation resulting from the interplay of blood platelets and contact activation was only found on surfaces combining both acidic and hydrophobic surface groups but not on monolayers displaying extreme hydrophobic/acidic properties.
生物材料诱导的凝血包括血浆和细胞过程。这些血栓反应可能导致生物医学设备的功能丧失，这促使人们需要更好地了解血液-生物材料界面上发生的过程。使用具有特定化学-物理性质（自组装单分子层 (SAM)）的定义明确的模型表面，展示疏水性和/或酸性末端基团，以揭示生物材料诱导的凝血的初始机制。我们研究了电荷和润湿性对血小板和接触激活的影响，这是血液凝固的两个主要因素，在生物材料研究中通常被认为是两个独立的机制。我们的结果表明接触激活依赖于酸性表面基团，血小板黏附与表面疏水性相关。只有在同时具有酸性和疏水性表面基团的表面上，才会发现由血小板和接触激活相互作用形成的血栓，而在具有极端疏水性/酸性性质的单层上则不会。
