QUANTITATION OF PLATELET DEPOSITION ON HUMAN ARTERIES - ASSESSMENT OF THE DISPARITY BETWEEN RESULTS OBTAINED WITH INDIUM-111(IN-111)-LABELING 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 In-111-scintigraphy. Part of this disparity may be explained by nonspecific binding of In-111 to the vessel surface during perfusion, or loss of adherent In-111-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 In-111 retention. Of the total In-111 that bound to the vessel surface during perfusion, 77 +/- 42% (N=9) was platelet associated In-111 (In-111-labelled platelets) and 23 +/- 19% (N=9) was non-platelet associated In-111 (nonspecific binding). After specimen fixation, 67 +/- 32% (N=9) of the initial total surface In-111 remained. This decrease is due to dissociation of both adherent In-111-labelled platelets, and non-platelet associated In-111. After fixation, 57 +/- 34% (N=9) of the initial total surface In-111 remained as In-111-labelled platelets and 10 +/- 13% (N=9) remained as non-platelet associated In-111. Fixation caused no measurable lysis of platelets. These data suggest that PD may be overestimated by In-111-scintigraphy because of nonspecific binding of In-111 and underestimated by SEM because of dissociation of adherent platelets during specimen preparation for SEM.