Rifampicin-containing interpenetrating hydrogel networks (IHNs) based on poly(methacrylates) and Poloxamers, and their potential as short-duration use antimicrobial medical device biomaterials.

This study describes the surface, mechanical, swelling, microbial anti-adherence and drug release properties of rifampicin-containing interpenetrating hydrogel networks (IHNs) composed of either poly(hydroxyethylmethacrylate, p(HEMA)) or poly(methacrylic acid, p(MAA)) and Poloxamer block copolymers (grades F127, P123 and L121), prepared using free radical polymerisation and designed as coatings for urinary medical devices. The swelling and mechanical properties of the IHNs were affected by the polymethacrylate type, Poloxamer grade and concentration. Incorporation of Poloxamers decreased the crosslink density and increased the pore size of the hydrogels at pH 7.2 (calculated from swelling data), leading to enhanced IHN swelling and reduced ultimate tensile strength and Young's Modulus. The static contact angles of the IHNs depended on the type of polymethacrylate but not on the Poloxamer grade/concentration. In particular, the contact angles of p(HEMA) IHNs were greater than for p(MAA) IHNs. The contact angles of p(MAA) IHNs at pH 4 were greater than those at pH 7.2. ATR-FTIR confirmed the presence of PEO at the surface of p(MAA)/F127 IHNs. Drug loading into (by swelling) and subsequent release at pH 7.2 buffer depended on polymethacrylate type, grade and concentration of Poloxamers. Rifampicin release from p(MAA) IHNs was significantly greater than from comparator p(HEMA) IHNs, due to both the greater loading of rifampicin and the increased pore size of these hydrogels. The mass of rifampicin loaded into the hydrogels was greater for p(MAA) IHNs Release of rifampicin from p(MAA) hydrogels at pH 4 (pre-swollen in rifampicin solutions at pH 7.2) involved burst release (dependent on and reduced by increasing concentration of Poloxamer), followed by slow, controlled release, again affected by Poloxamer concentration. p(HEMA) p(HEMA) IHNs significantly decreased microbial adherence, with the inclusion of rifampicin inhibiting microbial adherence at 4 h (for selected IHNs) and 24 h. Microbial adherence to rifampicin-containing p(MAA) IHNs following a 4-hour contact time was inhibited; however, given the rapid drug release, prolonged anti-adherence is unlikely. Conversely, the ability of Poloxamers to enhance and offer both greater control of rifampicin release from p(HEMA) IHNs and the more prolonged anti-adherence effects make these platforms more suitable for urinary application.