Development of polymer systems capable of counteracting surface-induced fibrillogenesis

It is known that the use of medical devices having polymer surfaces exposed to blood flow often leads to thrombogenesis. The mechanism of thrombus formation depends, in part, on the hydrophobic/hydrophilic nature and adhesive properties of the surface, on which spontaneously initiated fibrillogenesis can occur in the absence of thrombin. In this work, the connection between the “Berg limit” and the ability of polymer surfaces to aggregate fibrinogen into fiber structures was investigated using two unique systems. Polystyrene (PS), a well-characterized, stable polymer, was first tested because of its ability to readily impart hydrophilicity using UV-ozone without additional additives. However, in order to explore a biodegradable polymer with greater physiological relevance, the focus was switched to polyvinyl alcohol (PVA). To improve the mechanical properties and increase the hydrophilicity of PVA, a chemical approach was used with the addition of the clay functionalized with resorcinol diphenyl phosphate (RDP). Observations for the two different systems indicated that fibrinogen absorption undergoes a transition through the Berg limits, regardless of a physical or chemical approach, and that there was a significant reduction in surface fibrillogenesis with contact angles below this threshold. Finally, HUVEC cell adhesion to the surface of PVA-RDP with no negative effect on proliferation and endothelialization capability was demonstrated. A guideline is proposed for designing non-thrombogenic materials by rendering the surface hydrophilic. This phenomenon could be applied to engineering polymers more applicable to biomedical purposes.