The effects of substrate-adsorbed albumin on platelet spreading

Adsorbed albumin appears to passivate nearly all materials, minimizing platelet adhesion and thrombus formation. Since in vitro platelet spreading can be an indicator of in vivo reactivity leading to thrombosis, and as in vitro platelet adhesion investigations are routinely done in the presence of bovine or human serum albumin (BSA or HSA), we examined the influence of albumin on platelet reactivity to material substrates. Platelet spreading was examined subsequent to adherence onto several related polyurethanes, and to Formvar, in the presence of bulk albumin concentrations sufficient to form an adsorbed monolayer or a multilayer. No other exogenous proteins were present. The spreading behavior of adherent platelets was analyzed using generalized linear interactive modeling (GLIM). The models showed that the polymer type always influenced platelet responses, irrespective of the albumin concentration. In many experiments, platelet behavior could be adequately modeled without including the effects of albumin. Thus, the polymer type appeared to be the primary determinant of platelet shape-change with adsorbed albumin producing a secondary effect. Additionally, somewhat different effects on spreading were observed with HSA and BSA, suggesting qualitatively different interactions between human platelets and HSA, than with BSA, which is commonly used in platelet preparations.