Grace H. Nguyen, Mark Garren, Vicente Pinon, McKenna Clary, Hitesh Handa, Elizabeth J. Brisbois
Implanted medical devices frequently trigger infection, thrombosis, and surface fouling, creating a critical need for new surface-based strategies that reduce biological complications without systemic drugs. Typically, patients receive treatment for these complications, with the more invasive treatments inherently carrying a greater risk for infection, thrombosis, and adverse events, especially with blood-contacting medical devices. With higher risks and incidence rates of infections and blood clots, patients experience longer hospitalizations that would otherwise not occur. Therefore, the need for more effective preventive and treatment strategies is increasingly evident in the research literature. Anti-fouling surface coatings, particularly those that prevent biomolecule accumulation and bacterial attachment, have emerged as a promising alternative to systemic antimicrobial and anticoagulant therapies. In this work, the aliphatic, thiolated lubricant tert-dodecylmercaptan was nitrosated (SNTDM), diluted with n-hexadecane (C16), and incorporated into crosslinked polydimethylsiloxane (PDMS) in a facile impregnation method to render the substrate nitric oxide (NO)-releasing and slippery. The n-hexadecane/SNTDM-swelled samples exhibit slippery behavior with sliding angles <20° while releasing physiological levels of NO for up to 14 d. The samples with n-hexadecane did not elicit cytotoxic responses from human BJ fibroblasts while still significantly reducing the viable number of Escherichia coli and Staphylococcus aureus by 1.97 and 1.70 log, respectively. The 16% SNTDM-C16 sample also demonstrated effective reduction of adsorbed fibrinogen and adhered platelets by ∼39.17% and 67.5%, respectively. Together, these results demonstrate that SNTDM/n-hexadecane-infused PDMS provides a simple but effective strategy for fabricating NO-releasing slippery surfaces that significantly reduce bacterial viability, fouling, and thrombogenic responses.