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.