Thrombosis and infection are two major complications associated with cardiovascular devices such as ventricular assist devices, total artificial hearts, vascular grafts, and catheters. When blood contacts an artificial biomaterial, protein deposition occurs, as do activation of the blood coagulation cascade, platelet adhesion, activation, and aggregation, all of which lead to thrombus formation. An increased incidence of bacterial infection also has been seen clinically with indwelling biomaterial devices. Some evidence suggests a possible association between thrombosis and infection, in that adherent bacteria may provide a nidus for thrombus formation, or adherent thrombi composed of platelets and fibrin may form sheltered sites for bacterial adhesion.1,2 In the current study, the authors examined Staphylococcus aureus adhesion to sulfonated, aminated, and phosphonated polyurethane surfaces that had been pre-adsorbed with solutions of increasing complexity, in an effort to approach and simulate clot formation on the surface. These solutions included various combinations of fibrinogen, albumin, plasma, thrombin, and isolated platelets. Bacterial adhesion was observed in a radial flow chamber mounted on the motorized stage of a video microscopy system, with image processing software used to perform automated data collection and image analysis. Scanning electron microscopy also was used to visualize cross-linked fibrin and bacterial adhesion on these surfaces. Bacterial adhesion was found to be lowest on the phosphonated polyurethane. The presence of fibrin or isolated platelets significantly increased bacterial adhesion compared to surfaces pre-adsorbed with albumin.
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