Surface coating of polyurethane films with gelatin, aspirin and heparin to increase the hemocompatibility of artificial vascular grafts

Aim and Background: This study aimed to develop a hemocompatible substrate for nitric oxide (NO) production by vascular endothelial cells following inflammation from injuries. NO plays a critical role in inhibiting platelet aggregation, especially in small-diameter vessels. Methods: Polyurethane (PU) films were cast and surface-modified with polyethylene glycol (PEG) 2000, gelatin, gelatin-aspirin, gelatin-heparin, and gelatin-aspirin-heparin after plasma treatments. The concentrations of the ingredients were optimized for biocompatibility, and the modifications were characterized by water contact angle and Fourier Transform Infra-Red (FTIR) assays. The study examined NO production and platelet adhesion. Results and discussion: The water contact angle of the modified surface was reduced to 26 ± 4⸰, and the FTIR confirmed the newly developed hydrophilic chemical groups. The IC50 values of aspirin and heparin were determined to be 0.05 mg/ml and 100 mg/ml, respectively. The bioactivity of the substrate increased after surface modification with aspirin compared to other experimental groups. There was also a synergistic effect between these reagents for NO synthesis. Heparin inhibited platelet adhesion more than aspirin due to its highly hydrophilic nature. Conclusion: The study provides the biocompatible concentrations of both biomolecules required for endothelial cell proliferation, NO synthesis, and platelet adhesion. Aspirin and heparin have a synergistic effect on NO production, with heparin showing more significant inhibition of platelet adhesion due to its faster hydrolysis rate. The modified PU films may provide a hemocompatible substrate for NO production and inhibition of platelet aggregation in small-diameter vessels following injury. The study results provide a promising approach to controlling vascular wall thickness.