Clotting Phenomena at the Blood-Polymer Interface and Development of Blood Compatible Polymeric Surfaces

In the past two decades many attempts have been made to relate surface and interfacial parameters with the blood compatibility of polymeric surfaces. It is however doubtful if by a single parameter the behaviour of blood on a surface can be predicted. Two major aspects of blood compatibility - the prevention of platelet adhesion and the deactivation of the intrinsic coagulation system are determined by the measure and nature of competitive blood protein adsorption on the foreign surface. The adhesion of blood platelets is promoted by adsorbed fibrinogen and gamma globulin, while adsorbed albumin inhibits platelet adhesion. Heparinised surfaces do not adsorb fibrin and consequently no adhesion of platelets takes place. Other surfaces with low platelet adhesion are the hydrogels, certain block copolyetherurethanes, polyelectrolyte complexes and biolised proteins. Heparinised surfaces of the cationically bonded type inhibit the intrinsic coagulation as well, however this may be due to unstable coatings and heparin leakage. In the authors laboratory a synthetic heparinoid was prepared with the structure - [CH2 - C(CH3 NHSO3 Na - C(H) COONa - CH2 -]x with Mw = (7.5 /pm 1.0) × 105 and an in vivo anticoagulant activity of 50% of heparin. Its coatings on PVC, using tridodecylmethyl-ammonium chloride as a coupling agent, are stable in plasma and salt solutions and provide surfaces which show negligible platelet adhesion and a strong inhibition of the intrinsic coagulation on contact with blood. Similar results were found with polydimethylsiloxane surfaces coated with this heparinoid.