Healthcare-associated infections are a serious concern, particularly in patients with intravascular catheters. In this study, we developed a novel ampicillin-loaded polycaprolactone (PCL)-coated polyurethane catheter (PUC) wherein polymethylhydrosiloxane (PMHS) enhanced the adhesion between PCL and PUC, ensuring coating durability. PUC were first treated with PMHS, followed by PCL coatings containing 1, 3, or 6 wt% ampicillin. Antibacterial activity against Listeria innocua and Escherichia coli was evaluated using the plate counting method over 40 d. Scanning electron microscopy confirmed that the coating was uniform and stable for over 40 d. Furthermore, antibacterial efficacy was maintained for 10, 30, and 40 d for the 1, 3, and 6 wt% ampicillin coatings, respectively. Compared to the uncoated controls, the bacterial counts were reduced by over 99.9%. Thus, PMHS pretreatment of a catheter coated with ampicillin-loaded PCL exhibited sustained antibacterial activity. Our findings show PMHS enhances the coating adhesion and ensures gradual uniform degradation of the PCL layer.

The systemic inflammatory response syndrome can occur due to an inflammatory reaction to the release of cytokines, and it has been linked to the circulation of pro- and anti-inflammatory cytokines. The cardiopulmonary bypass (CPB) system is known to activate numerous inflammatory pathways. Applying CPB in large animals for an extended period may be useful as a controlled experimental model for systemic inflammatory responses. The authors hypothesized that 0.2 mg/kg NuSepin^® would inhibit CBP-induced proinflammatory cytokine release, and attenuate CPB-induced vasoplegia. CPB was maintained for 2 h in 8 male Yorkshire pigs. Ten ml of saline was administered intravenously to the control group, while the study group received 10 ml of NuSepin^® (0.2 mg/kg), before start of CPB. Blood samples were collected at four different time points to evaluating the level of cytokine (TNF-α, IL-1β, IL-6, IL-8) release during and after CBP. All vital signals were recorded as continuous waveforms using the vital recorder^®. Our study demonstrated that IL-6 increased in both groups during CPB remained unchanged. However, in the Nusepin group, IL-6 levels rapidly decreased when CPB was stopped and the proinflammatory reaction subsided. Furthermore, the dose of norepinephrine required to maintain a mean pressure of 60 mmHg was also lower in the Nusepin group.