EDTA-induced changes in platelet structure and function: clot retraction

Ethylenediamine tetracetic acid (EDTA) is known to cause structural, bioche mical and functional injury to blood platelets, including irreversible diss ociation of the fibrinogen receptor, glycoprotein alpha(IIb)beta(3) (GPIIb/ IIIa), Despite inability to adhere to glass, spread, and to aggregate in re sponse to adenosine diphosphate (ADP) and other agonists, EDTA-treated plat elets support clot retraction as well as untreated cells. The present study has used clot retraction under isometric tension and electron microscopy t o determine if there are any differences in platelet-fibrin interactions of clots formed from blood collected in EDTA or platelets from blood drawn in to citrate (CCD) anticoagulants. No physical differences could be identifie d. Polymerizing fibrin bound intimately to aggregates developing from EDTA platelets undergoing shape change, internal transformation, adhesion and sp reading on fibrin strands oriented in the long axis of contraction. The res ults suggest that reassociation of irreversibly dissociated GPIIb/IIIa take s place immediately after initiation of clot retraction, or that a signific ant proportion of GPIIb/IIIa receptors on resting platelets are inaccessibl e to EDTA and become available after activation by thrombin.