Platelet adhesion onto a polystyrene surface under static conditions: role of specific platelet receptors and effect of divalent cations.

An experimental model was used to elucidate the basic mechanisms involved in the interaction of platelets with an artificial surface. The role of divalent cations and the involvement of specific platelet membrane receptors were evaluated. Isolated platelets were allowed to interact with a polystyrene surface for 20 min in the presence of divalent cations (Ca2+, Mg2+ or Zn2+), a chelating agent (ethylenediaminetetraacetic, EDTA), and specific antibodies to the main platelet receptors, glycoproteins (GP) Ib and IIb-IIIa. The degree of platelet interaction was evaluated using light and electron microscopy. Morphometric analysis was performed to follow up the progression of platelet shape changes after surface activation. Neither Ca2+ nor Mg2+ influenced the number of adherent platelets or the degree of spreading on the polymer. Only Zn2+ induced a statistically significant increase in the rate of platelet adhesion (P<0.01) with higher proportion of fully spread platelets (P<0.01). Chelation of internal pools of divalent cations did not modify the rates of platelet adhesion but prevented platelet spreading. Presence of monoclonal antibodies to GPIb and GP IIb-IIIa did not result in significant differences in the studied parameters. These results suggest that platelet adhesion onto artificial surfaces, in the absence of flow and plasma proteins, is more dependent on cellular motility, where Zn2+ could play an important role, and less dependent on major receptorial mechanisms.