Disease relevance of Blood Vessel Prosthesis

• Protective effect of warfarin in arterial thrombosis: evidence from a vascular prosthesis model in rats [1].
• Neointimal fibromuscular hyperplasia (NFH) in vein grafts and perianastomotic zones of vascular prostheses has been attributed to the effects of platelet-derived growth factor (PDGF) released by platelets interacting with bypass conduits [2].
• Blood hemolysis by PTFE and polyurethane vascular prostheses in an in vitro circuit [3].
• The contraindication to curative excision of mediastinal and pulmonary cancers because of invasion of the superior vena cava is now challenged by the existence of vascular prostheses that are suitable for venous replacement [4].
• It is not known whether the antimicrobial agent triclosan induces a significant acute phase reaction when bonded to vascular prostheses [5].

High impact information on Blood Vessel Prosthesis

• A vascular prosthesis needs angiogenesis for endothelialization of the luminal surface, as endothelial cells have natural and permanent antithrombogenic properties [6].
• Implanted vascular prostheses generate prostacyclin [7].
• The balloon-expandable vascular prosthesis consists of a flexible, knitted tantalum wire mesh tube [8].
• Tissue plasminogen activator labeled with radioactive iodine (125I-tPA) was immobilized on vascular prostheses chemically modified with a thin coating of water-insoluble surfactant, tridodecylmethylammonium chloride (TDMAC) [9].
• The time of occlusion of the vascular prosthesis was significantly prolonged when warfarin was started 24 hr previously, at the time of loop insertion or 24 hr later [1].

Chemical compound and disease context of Blood Vessel Prosthesis

• On the luminal surface of the common synthetic vascular prostheses, blood coagulation can occur and a thrombus membrane is formed when blood flow passes through it [10].
• The acute phase response following implantation of triclosan-bonded vascular prostheses [5].

Biological context of Blood Vessel Prosthesis

• Nitric oxide prevents the bacterial translocation and inhibits the systemic inflammatory response produced by implantation of a vascular prosthesis followed by Zymosan A [11].
• These results indicate that the simple adsorption of bFGF onto Dacron fabric is a useful method for the acceleration of host cell migration and capillary ingrowth into Dacron fabric vascular prostheses [12].
• In conclusion, the circulating CD34(+) cell counts and serum VEGF levels are increased after vascular prosthesis replacement in patients with aortic aneurysm, which might contribute to the rapid endothelialization of prosthetic vessels [13].

Anatomical context of Blood Vessel Prosthesis

• To study the effect of haemodynamic stress on the morphological differentiation of pseudointima, the ultrastructure of the cells lining normally shaped and aneurysmal polyurethane vascular prostheses implanted into the abdominal aorta of rats was examined [14].
• Three different vascular prostheses (standard weight knitted Dacron, double velour knitted Dacron, and expanded polytetrafluoroethylene) were implanted in the aortas of dogs, and serial determinations of platelet survival and platelet serotonin were monitored at 12-week intervals for 1 year [15].
• To evaluate the biocompatibility of chemically and structurally modified polyurethane elastomers for use as blood vessel replacements, small squares of vascular prostheses were cultured in direct contact with endothelium from chick embryo aorta using an organotypic culture assay [16].
• Polytetrafluoroethylene (PTFE) and polyethylene terephthalate (Dacron polyester) fabrics are used extensively in cardiovascular devices, e.g. heart valve sewing cuffs and vascular prostheses [17].
• Transmural endothelialization of vascular prostheses is regulated in vitro by Fibroblast Growth Factor 2 and heparan-like molecule [18].

Associations of Blood Vessel Prosthesis with chemical compounds

• Polyurethane vascular prostheses decreases neointimal formation compared with expanded polytetrafluoroethylene [19].
• A comparison of isobutyl 2-cyanoacrylate glue, fibrin adhesive, and oxidized regenerated cellulose for control of needle hole bleeding from polytetrafluoroethylene vascular prostheses [20].
• Polyglactin 910/polydioxanone bicomponent totally resorbable vascular prostheses [21].
• The deposition of indium 111-labeled platelets on the vascular prostheses was studied 1 and 4 months after operation [22].
• Heparin coating of vascular prostheses reduces thromboemboli [23].

Gene context of Blood Vessel Prosthesis

• Rupture of pseudointima in an implanted vascular prosthesis: immunohistological study of plasminogen activators and matrix metalloproteinases [24].
• Sustained release of basic fibroblast growth factor from the synthetic vascular prosthesis using hydroxypropylchitosan acetate [25].
• We designed a model vascular prosthesis consisting of expanded polytetrafluoroethylene (Gore Tex) loaded with basic fibroblast growth factor (bFGF), and studied its in vivo bFGF release behavior [25].
• After seeding MVEC on vascular prostheses, TM activity did not change [26].
• When seeded on ePTFE, MVEC retain the possibility to inhibit thrombin coagulant activity and to activate protein C. Therefore, since MVEC are readily available, the anticoagulant properties demonstrated here indicate that this cell type is suitable for cell seeding of vascular prostheses [26].

Analytical, diagnostic and therapeutic context of Blood Vessel Prosthesis

• This study was designed to assess platelet activity in vivo with vascular prostheses seeded with endothelial cells to determine the time course for development of thromboresistance and to test the ability of prostheses to produce prostacyclin [27].
• In seeded venous vascular prostheses, light, scanning, and transmission electron microscopy showed emergence of numerous flattened endothelial cell-like cells on the luminal surface 24 hours after surgery, followed by formation of a confluent cellular lining without adherent platelets by 5 to 10 days after surgery [28].
• This study, using C3a, C4a, and C5a assay and crossed immunoelectrophoresis in vitro and in vivo, was designed to determine whether vascular prostheses activate the complement system [29].

References