Summary
In cat brain with a freezing injury, the uptake of 1-11C-acetoacetate (11C-ACAC), 2-18F-fluorodeoxy-D-glucose (18FDG), and L-1-11C-tyrosine (11C-TYR) was monitored by positron emission tomography following intravenous administration of the tracers, at 1 day and 1–3 weeks after the injury. The development and further course of the cold-induced oedema was monitored by magnetic resonance imaging. In the fresh (1 day old) lesion there was increased uptake of11C-ACAC, probably due to release of the restrictive influence of the blood-brain barrier upon passage of the substance into brain. The uptake of18FDG, which normally occurs by carrier-mediated transport at the barrier, was decreased in the fresh lesion, probably as a result of damage of the carrier mechanism. In the 3 week old lesion18FDG uptake was still reduced, and11C-ACAC uptake was still increased, although barrier function to Evans blue had recovered. It is suggested, that the increased11C-ACAC uptake in the chronic lesion bears upon the proliferation of macrophages and reactive glial cells in the lesion. This is supported by the increased uptake of11C-TYR in the 2 weeks old lesion, while in the fresh lesion11C-TYR uptake was unchanged.
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Prenen, G.H.M., Go, K.G., Paans, A.M.J. et al. Positron emission tomographical studies of 1-11C-acetoacetate, 2-18F-fluoro-deoxy-D-glucose, and L-1-11C-tyrosine uptake by cat brain with an experimental lesion. Acta neurochir 99, 166–172 (1989). https://doi.org/10.1007/BF01402328
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DOI: https://doi.org/10.1007/BF01402328