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We have studied the kinetics, biodistribution, and fate of autologous platelets labeled with 111In-oxine in rabbits. The initial recovery was 75% and mean survival time was 2.8 days when the data were analyzed by the multiple-hit gamma function model. Using a modified geometric mean for correction of attenuation, there was good correlation between the values obtained by in vivo quantification and those obtained by postmortem measurements of the radioactivity in the liver and the spleen (i.e., r = 0.854 and 0.899, respectively, n = 32). Using this method, it was shown that after infusion, the 111In-platelets rapidly accumulated in these two organs reaching 35% and 12% of the injected dose in the liver and spleen, respectively, by 1 day. Thereafter, there was little subsequent change. On the sixth day, when essentially all of the 111In-platelets had cleared from the circulation, a total of 82% of the injected dose was deposited in the three major reticuloendothelial organs: liver (40%), spleen (14%), and bone marrow (28%). Our results suggest that in addition to liver and spleen, bone marrow played an important role in sequestering platelets in rabbits.

We have evaluated a method for quantitation of eosinophil migration to stimuli in vivo. Upon transfusion into normal syngeneic mice, 111In-labeled eosinophils had an intravascular half-life of 9.5 hr and distributed predominantly into spleen, bone marrow, and liver. In either Schistosoma mansoni-infected mice or recipients of lymphoid cells from infected mice, intradermal (ear pinna) injection of the schistosomal egg antigenic preparation (SEA) elicited time-dependent accumulation of 111In-labeled eosinophils detectable by either gamma scintillation counting of tissue samples or by nuclear medicine external imaging. Intradermal administration of a lymphokine fraction (containing eosinophil stimulation promoter activity) similarly caused accumulation of 111In-labeled eosinophils. Both reactions depended on the concentration of stimulus (SEA or lymphokine). 111In-labeled neutrophils or macrophages or 125I-albumin did not preferentially accumulate at the reactions examined to the extent found with 111In-labeled eosinophils, indicating that localization of label depends on an active process and is due to eosinophils rather than a contaminating cell type. The method was used to estimate how long eosinotactic lymphokine remained at dermal sites: 60% of initial activity was present 12 hr after injection. The model is discussed with regard to the role of lymphokines in hypersensitivity reactions with eosinophil involvement, such as the granulomatous response to S. mansoni eggs.