Preliminary evaluation of [1-C-11]octanoate as a PET tracer for studying cerebral ischemia: A PET study in rat and canine models of focal cerebral ischemia

Citation
Y. Kuge et al., Preliminary evaluation of [1-C-11]octanoate as a PET tracer for studying cerebral ischemia: A PET study in rat and canine models of focal cerebral ischemia, ANN NUCL M, 14(1), 2000, pp. 69-74
Citations number
33
Categorie Soggetti
Radiology ,Nuclear Medicine & Imaging
Journal title
ANNALS OF NUCLEAR MEDICINE
ISSN journal
09147187 → ACNP
Volume
14
Issue
1
Year of publication
2000
Pages
69 - 74
Database
ISI
SICI code
0914-7187(200002)14:1<69:PEO[AA>2.0.ZU;2-B
Abstract
Octanoate is taken up into the brain and is converted in astrocytes to glut amine through the TCA cycle after beta-oxidation. We speculate that [1-C-11 ]octanoate may be used as a tracer for astroglial functions and/or fatty ac id metabolism in the brain and may be useful for studying cerebral ischemia . In the present study we investigated brain distribution of [1-C-11]octano ate and compared it with cerebral blood flow (CBF) by using rat and canine models of middle cerebral artery (MCA) occlusion and a high resolution PET. In rats brain distribution of [O-15]H2O measured 1-2 h and 5-6 h after ins ult was compared with that of [1-C-11]octanoate measured 3-4 h after insult . Radioactivity ratios of lesioned to normal hemispheres determined with [O -15]H2O were lower than those determined with [1-C-11]octanoate. These resu lts were confirmed by a study on a canine model of MCA-occlusion. Twenty-fo ur hours after insult, CBF decreased in the MCA-territory of the occluded h emisphere, whereas normal or higher accumulation of [1-C-11]octanoate was o bserved in the ischemic regions. The uptake of [1-C-11]octanoate-derived ra dioactivity therefore increased relative to CBF in the ischemic regions, in dicating that [1-C-11]octanoate provides functional information different f rom CBF. In conclusion, we found that [1-C-11]octanoate is a potential radi opharmaceutical for studying the pathophysiology of cerebral ischemia.