Thrombin uptake and inhibition on heparinized polytetrafluoroethylene (PTFE) grafts and native sheep vessels.
Non-heparinized and covalently-heparinized PTFE grafts, sheep aorta, carotid artery and jugular vein were evaluated according to their ability to adsorb and inactivate thrombin. All surfaces, except non-heparinized PTFE caused considerable losses of enzymatically active thrombin from the solution. Covalently-heparinized PTFE and jugular veins adsorbed thrombin, which was inactivated on subsequent contact with antithrombin III. Despite the same loss from the solution as was encountered with veins arteries adsorbed significantly smaller amounts of thrombin. Protamine treatment of covalently-heparinized PTFE almost totally abolished the ability to adsorb thrombin. It is concluded that 1) arteries possess a stronger thrombin inhibitory capacity than veins, possible explanations to this being a different glucosaminoglycan or the presence of antithrombin III in the arterial wall and 2) that heparinizing PTFE results in a pronounced ability to inactivate thrombin.
D000818:Animals; D001011:Aorta / Q000502:physiology / Q000648:ultrastructure; D001807:Blood Vessel Prosthesis; D001808:Blood Vessels / Q000378:metabolism / Q000502:physiology*; D002339:Carotid Arteries / Q000502:physiology / Q000648:ultrastructure; D002473:Cell Wall / Q000378:metabolism; D006493:Heparin / Q000502:physiology*; D006801:Humans; D066298:In Vitro Techniques; D007601:Jugular Veins / Q000502:physiology / Q000648:ultrastructure; D011138:Polytetrafluoroethylene / Q000502:physiology / Q000627:therapeutic use*; D011485:Protein Binding; D012756:Sheep; D013917:Thrombin / Q000037:antagonists & inhibitors / Q000378:metabolism*
D011138:Polytetrafluoroethylene; D006493:Heparin; D013917:Thrombin