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The first major event when a medical device comes in contact with blood is the adsorption of plasma proteins. Protein adsorption on the material surface leads to the activation of the blood coagulation cascade and the inflammatory process, which impair the lifetime of the material. Various efforts have been made to minimize protein adsorption and platelet adhesion. Recently, diamond-like carbon (DLC) has received much attention because of their antithrombogenicity. We recently reported that coating silicon substrates with fluorine-doped diamond-like carbon (F-DLC) drastically suppresses platelet adhesion and activation. Here, we evaluated the protein adsorption on the material surfaces and clarified the relationship between protein adsorption and platelet behaviors, using polycarbonate and DLC- or F-DLC-coated polycarbonate. The adsorption of albumin and fibrinogen were assessed using a colorimetric protein assay, and platelet adhesion and activation were examined using a differential interference contrast microscope. A higher ratio of albumin to fibrinogen adsorption was observed on F-DLC than on DLC and polycarbonate films, indicating that the F-DLC film should prevent thrombus formation. Platelet adhesion and activation on the F-DLC films were more strongly suppressed as the amount of fluorine doping was increased. These results show that the F-DLC coating may be useful for blood-contacting devices.

Diamond-like carbon (DLC) is being considered for widespread clinical use as a surface coating for cardiovascular devices. We synthesized fluorinated DLC (F-DLC) coatings in order to create a more hydrophobic surface with improved antithrombogenicity and flexibility when compared with conventional DLC coatings by combining the inertness of DLC films with the advantage of fluorination. The purpose of this study was to evaluate the in vitro hemocompatibility and in vivo biocompatibility of the F-DLC coating for medical devices. The in vitro whole blood model confirmed that platelet loss was lower in the F-DLC group than in the noncoated group (SUS316L), which suggests the adhesion of a smaller number of platelets to F-DLC-coated materials. Furthermore, the biomarkers of mechanically induced platelet activation (beta-thromboglobulin) and activated coagulation (thrombin-antithrombin-three complex) were markedly reduced in the F-DLC-coated group. In vivo rat implant model studies revealed no excessive local and systemic inflammatory responses in the F-DLC group. The thickness of the fibrous tissue capsule surrounding the F-DLC-coated disk was almost equal to that of the noncoated SUS316L disk, which has the favorable biocompatibility for metallic implant materials. F-DLC coating thus appears to be a promising candidate for use as a coating material in blood-contacting devices.

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