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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 2.

Figure 2

Hyperoxic reperfusion leads to increased unmetabolized glucose and increased [3-13C]lactate in the hippocampus and cortex. A, The amount of unmetabolized 13C-glucose was significantly higher in the hippocampus and cortex of animals resuscitated under hyperoxic conditions compared with nonischemic controls. The trend toward increased unmetabolized [1-13C]glucose in animals resuscitated under normoxic conditions was not significant (P=0.1). B, Although not significant (P=0.06), there was a trend toward elevated 13C labeling in the C3 position of lactate in the hippocampus of animals reperfused under hyperoxic, but not normoxic, conditions compared with nonischemic controls. There was no difference in 13C incorporation into lactate in the cortex. Values are mean±SE for n=7 nonischemic controls, 7 hyperoxic animals, and 6 normoxic animals. *Significantly different from nonischemic controls; 1-way ANOVA with Tukey post hoc analysis, P<0.05.