Mechanisms for Reduced Fibrin Clot Formation on Liquid-Infused Surfaces

Biomedical devices are prone to blood clot formation (thrombosis), and liquid-infused surfaces (LIS) are effective in reducing the thrombotic response. However, the mechanisms that underpin this performance, and in particular the role of the lubricant, are not well understood. In this work, it is investigated whether the mechanism of LIS action is related to i) inhibition of factor XII (FXII) activation and the contact pathway; ii) reduced fibrin density of clots formed on surfaces; iii) increased mobility of proteins or cells on the surface due to the interfacial flow of the lubricant. The chosen LIS is covalently tethered, nanostructured layers of perfluorocarbons, infused with thin films of medical-grade perfluorodecalin (tethered-liquid perfluorocarbon), prepared with chemical vapor deposition previously optimized to retain lubricant under flow. Results show that in the absence of external flow, interfacial mobility is inherently higher at the liquid-blood interface, making it a key contributor to the low thrombogenicity of LIS, as FXII activity and fibrin density are equivalent at the interface. The findings of this study advance the understanding of the anti-thrombotic behavior of LIS-coated biomedical devices for future coating design. More broadly, enhanced interfacial mobility may be an important, underexplored mechanism for the anti-fouling behavior of surface coatings.