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SummaryHeparin-coated surfaces exhibit prolonged compatibility with blood in vitro and in vivo. Deposition of platelets occurs on heparinized surfaces and results in thrombocytopenia, if the surface area is sufficient. Interaction of platelets with heparin-coated materials appears to depend on a protein intermediate. Precoating of heparinized surfaces with fibrinogen solutions, platelet-free plasma, serum, or exhausted or bentonite-adsorbed plasma does not protect against platelet interaction but incubation in albumin reduces platelet adsorption. The behavior of platelets in respect to protein-coated heparinized surfaces parallels the selective adsorption of specific proteins by platelets in suspension.Previous reports from our laboratory have described a study of chemical bonding of heparin to hydroxyl bearing surfaces, such as cellophane, through the use of ethylene imine as an intermediate.'v2 Blood exposed to such surfaces exhibited a long whole blood clotting time that did not appear to result from desorbed heparin. The blood developed a defect in the intrinsic clotting system correctable by admixture of normal plasma. Collateral studies of adsorption of tritiated plasma proteins implied removal of protein clotting factors from the plasma by adsorption on the heparinized surfaces. The hypothesis was proposed that these surfaces owed their nonthrombogenicity to a passivating coat of plasma protein.*Markle Scholar. 69