The roles of plasma proteins in the adhesion of platelets and leukocytes to surfaces of artificial organs will be investigated further. Development and improvement of immunoradiometric assays (IRA) for detection and quantitation of plasma proteins adsorbed to materials will be continued and extended to other plasma proteins. A correlation between the adsorption and concentration of a plasma protein on an artificial surface detected by IRA and the adhesion of platelets, leukocytes, and erythrocytes will be studied by microscopic examination and by use of isotopically (111In, 51Cr, or 14C) labeled cells. Selected materials such as Cuprophane, poly(vinyl chloride), glass, Silastic rubber, polycarbonate, polystyrene will be used for these studies. Eventually, materials obtained from hemodialyzers, oxygenators, and other artificial organs used clinically will be investigated. A comparative study on the effects of various plasma proteins on the adhesion of platelets and leukocytes will be carried out by use of a centrifugation test (modified George test) or Richardson flow chamber test. Mechanisms responsible for the phenomena of how some proteins (e.g., fibrinogen) enhance platelet adhesion while inhibiting granulocyte adhesion, while other proteins (e.g., complement 3) enhance granulocyte adhesion but inhibit platelet adhesion will be investigated. Whether receptor(s) or bindng sites on the plasma membranes of platelets and leukocytes are involved in the mediation of cell-material interactions by certain plasma protein will be probed. A hypothesis that leukocyte adherence to material may cause the subsequent activation of platelets with their adherence to the same material (or vice versa) will be tested. Effects of prostaglandins (PGs) (e.g., PGE1, PGI2) on the adhesion of platelets and leukocytes mediated by plasma proteins will be studed. The possible control of platelet -, or leukocyte -material interactions by use of certain plasma proteins that inhibits cell adhesion, by use of surfaces passivated with plasma proteins or blood will be studied. Similarly, control of blood cell adhesion by use of anticoagulants or other pharmacologic agents, by use of PGs, or by use of inhibitors of PG synthetases will be examined. These studies are designed to increase our basic knowledge of the enhancing of inhibiting roles played by plasma proteins in the (Text Truncated - Exceeds Capacity)