Abstract
Polycarbonateurethanes (PCU) and polyetherurethanes (PEU) are used for medical devices, however their bio- and haemocompatibility is limited. In this study, the effect of titaniferous upgrading of different polyurethanes on the bio- and haemocompatibility was investigated by endothelial cell (EC) adhesion/proliferation and platelet adhesion (scanning electron microscopy), respectively. There was no EC adhesion/proliferation and only minor platelet adhesion on upgraded and pure PCU (Desmopan). PEUs (Texin 985, Tecothane 1085, Elastollan 1180A) differed in their cyto- and haemocompatibility. While EC adhesion depended on the type of PEU, any proliferative activity was inhibited. Additional titaniferous upgrading of PEU induced EC proliferation and increased metabolic activity. However, adherent ECs were significantly activated. While Texin was highly thrombotic, only small amounts of platelets adhered onto Tecothane and Elastollan. Additional titaniferous upgrading reduced thrombogenicity of Texin, preserved haemocompatibility of Elastollan, and increased platelet activation/aggregation on Tecothane. In conclusion, none of the PUs was cytocompatible; only titaniferous upgrading allowed EC proliferation and metabolism on PEUs. Haemocompatibility depended on the type of PU.
Highlights
Polyetherurethanes (PEU) and polycarbonaturethanes (PCU) are used in implantable medical devices because of their relatively superior biocompatibility and attractive mechanical properties [1,2,3,4,5]
The function of endothelialization and thromboresistance of medical device surfaces has been regarded as important means to improve their respective treatment effect
The maximal surface atom fraction of titanium (Ti) was between 19% and 21%, which decreased toward the inner part of the polyurethane
Summary
Polyetherurethanes (PEU) and polycarbonaturethanes (PCU) are used in implantable medical devices because of their relatively superior biocompatibility and attractive mechanical properties (high elongation capacity, good abrasion resistance, high flexibility, and good biocompatibility for short-term usage) [1,2,3,4,5]. Long-term contact-time of blood with artificial surfaces of medical devices such as small-caliber vascular grafts, heart valves, cardiac assist devices, and total artificial hearts increase the risk of thromboembolic complications that may lead to treatment failure. Endothelialization of the blood-contacting surfaces of medical devices would contribute to an antithrombogenic and anti-inflammatory coating that mimics the native lining of blood vessels and the heart [6]. Full coverage of polymer surfaces with endothelial cells (ECs) prevents platelet adhesion, thrombus deposition, inflammatory cell infiltration, and neointimal formation [7]. The function of endothelialization and thromboresistance of medical device (such as cardiovascular devices) surfaces has been regarded as important means to improve their respective treatment effect
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
