Quantitation of platelet deposition on human arteries: assessment of the disparity between results obtained with 111indium (111In)-labelling versus scanning electron microscopy.
Quantitation techniques for measuring platelet deposition (PD) to vessel surfaces are important to an understanding of thrombogenesis. In previous studies, scanning electron microscopy (SEM) has been shown to indicate a lower extent of PD than platelet 111In-scintigraphy. Part of this disparity may be explained by nonspecific binding of 111In to the vessel surface during perfusion, or loss of adherent 111In-labelled platelets by lysis or dissociation from the surface during specimen preparation for SEM. To assess whether these independent processes occur, we used a previously described human placental artery (HPA) perfusion model to quantify vessel 111In retention. Of the total 111In that bound to the vessel surface during perfusion, 77 +/- 42% (N = 9) was platelet associated 111In (111In-labelled platelets) and 23 +/- 19% (N = 9) was non-platelet associated 111In (nonspecific binding). After specimen fixation, 67 +/- 32% (N = 9) of the initial total surface 111In remained. This decrease is due to dissociation of both adherent 111In-labelled platelets, and nonplatelet associated 111In. After fixation, 57 +/- 34% (N = 9) of the initial total surface 111In remained as 111In-labelled platelets and 10 +/- 13% (N = 9) remained as nonplatelet associated 111In. Fixation caused no measurable lysis of platelets. These data suggest that PD may be overestimated by 111In-scintigraphy because of nonspecific binding of 111In and underestimated by SEM because of dissociation of adherent platelets during specimen preparation for SEM.