The antithrombotic effect of prostaglandin E1 immobilized on albuminated polymer matrix.

For intravascular implantation, a biofunctional surface seems to retard surface thrombosis upon synthetic materials. Prostaglandins, like PGI2, PGE1, and PGD2, etc., are believed to stimulate membrane-bound adenyl cyclase and thereby raise intracellular levels of c-AMP within platelets, which inhibit platelet adhesion and aggregation. A new procedure is suggested for the immobilization of prostaglandin E1 on an albuminated polymer matrix, through glutaraldehyde coupling. Materials thus prepared show dramatic antiplatelet effects, with regard to platelet adhesion, when compared with albumin-immobilized surfaces. The affinity of various modified surfaces toward platelet adhesion is studied, using washed platelets suspended in Tyrode's solution. Octane contact angle studies are used to develop an understanding of the varied nature of bound substrates at equilibrium on polymer surfaces. These are studied at the solid/liquid interface, which is closest to in vivo conditions. The plasma recalcification time demonstrates the anticoagulant properties of various surfaces. A possible role of PGE1 in reducing platelet activity in the presence and absence of vitamin C is discussed. This technique may be used in the development of non-thrombogenic surfaces on existing biomedical polymers. Simultaneous pharmaceutical modification of the blood with vitamin C may enhance the blood compatibility of the surface.