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. Author manuscript; available in PMC: 2008 Dec 12.
Published in final edited form as: Stroke. 2007 Apr 5;38(5):1578–1584. doi: 10.1161/STROKEAHA.106.473967

Figure 3.

Figure 3

Hyperoxic reperfusion decreases hippocampal but not cortical metabolism of [1-13C]glucose to 13C-glutamate. A, Metabolism of [1-13C]glucose to glutamate but not glutamine is decreased in the hippocampus of animals resuscitated under hyperoxic conditions after a 10-minute cardiac arrest and 2-hour reperfusion paradigm. Decreased incorporation of 13C into glutamate C4 indicates decreased oxidative metabolism in neurons, possibly due to decreased PDHC activity and TCA cycle metabolism. Decreased labeling in the C2 of glutamate indicates impaired metabolism via the pyruvate carboxylase pathway in astrocytes. B, In the cortex, there was no difference in metabolism of 13C-glucose to either glutamate or glutamine after ischemia/reperfusion. Values are mean±SE for n=7 nonischemic controls, 7 hyperoxic animals, and 6 normoxic animals. *Significantly different from nonischemic controls; ANOVA with Tukey test, P<0.05.