Octanoate is taken up by the brain and converted in astrocytes to glutamine through the TCA cycle after beta-oxidation. Consequently, [1-11C]octanoate might serve as a useful positron emission tomography (PET) probe for studying cerebral oxidative metabolism and/or astroglial functions. The present study attempted to evaluate the utility of using [1-11C]octanoate as a PET tracer for imaging and evaluating the pathophysiology of ischemic stroke. We used a canine model of thromboembolic stroke. Five male beagle dogs were implanted with an indwelling catheter in the left internal carotid artery. A single autologous blood clot was injected into the left internal carotid artery through the catheter. The brain distribution of [1-11C]octanoate and cerebral blood flow (CBF) were determined 24 h after insult using a high resolution PET scanner. Post mortem brain regions unstained with 2,3,5-triphenyltetrazolium chloride (TTC) were defined as infarcts. In the region of an infarct, accumulation of [1-11C]octanoate decreased concurrently with CBF reduction. In contrast, normal accumulation of [1-11C]octanoate was observed in ischemic but vital regions, suggesting that an increased accumulation of [1-11C]octanoate relative to CBF takes place in these regions. In conclusion, [1-11C]octanoate accumulated in ischemic but vital regions, indicating that [1-11C]octanoate is a potentially useful PET tracer for imaging and evaluating the pathophysiology of ischemic stroke.