Studies of the vivo uptake of Ga-67 by an experimental abscess: concise communication.
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.[1]References
- Studies of the vivo uptake of Ga-67 by an experimental abscess: concise communication. Hayes, R.L., Rafter, J.J., Carlton, J.E., Byrd, B.L. J. Nucl. Med. (1982) [Pubmed]
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