The blocking of Ga -67
plasma protein-binding sites-by administration of
scandium citrate,
ferric citrate, and a colloidal hydrous
ferric oxide preparation-reduced the uptake of Ga-67 in normal soft tissues and also that in the viable portion of an experimental
abscess. On the other hand, enhancement of Ga-67
plasma protein binding by administration of rabbit
apotransferrin increased Ga-67 uptake in both
abscess and normal soft tissues. These results indicate that the pathways of Ga-67 from blood into inflammatory processes and normal soft tissues may be similar. However, when Ga-67
plasma protein binding was increased by inducing
anemia, a markedly decreased Ga-67 uptake in the
abscess resulted, whereas uptake in normal soft tissue was still elevated. It is possible that the discrepancy between the effects of
apotransferrin and
anemia on
abscess-tissue uptake of Ga-67 resulted from a secondary effect produced by
anemia, i.e., a decrease in the macrophage population in the
abscess. Taken as a whole, the results obtained suggest that Ga-67 leaves the blood and enters inflammatory lesions by pathways that are probably quite different from those in a soft-tissue
tumor, and that the routes for
abscesses may be similar to those occurring in normal soft tissues.