Fig. 5.
Changes in neuronal–glial metabolites for all three time points and all three treatment groups: normothermia, hypothermia, and 15-min delayed hypothermia, represented by “N”, “H”, and “D,” respectively. In graphs B–Gx axis represents time points, and y axis represents the ratio of each time point to initial time. (A) Ratios for the end of recovery (T3) of pyruvate carboxylase (PC)/(pyruvate dehydrogenase (PDH) fluxes producing 13C-glutamate and 13C-glutamine, calculated from (C2 − C3)/C4 of glutamate or glutamine. Calculated values have no relation to control values at T0, and are not normalized to them. In the text there is a discussion of group H’s significantly greater PC/PDH for glutamine production. (B) Ratios of acetate/glucose consumption glutamate production, which at the end of the recovery period was significantly decreased in group D. Values for each time point are normalized to T0 control data. (C–G) Metabolite quantifications for the last three time points, each measured relative to T0 control data. (C) Glutamate C2; (D) glutamine C2, which was always increased in the hypothermia group; (E) lactate C3; (F) glutamate C4, and (G) glutamine C4; (H) fractional 13C enrichment of lactate came from 1H data at 1.33 ppm, and was not normalized to control values. All data are presented as mean ± standard error values for three experiments. Significant differences, highlighted with asterisks, are defined with P < 0.0056, the Bonferroni-corrected upper limit 5% for type I errors.

Changes in neuronal–glial metabolites for all three time points and all three treatment groups: normothermia, hypothermia, and 15-min delayed hypothermia, represented by “N”, “H”, and “D,” respectively. In graphs BGx axis represents time points, and y axis represents the ratio of each time point to initial time. (A) Ratios for the end of recovery (T3) of pyruvate carboxylase (PC)/(pyruvate dehydrogenase (PDH) fluxes producing 13C-glutamate and 13C-glutamine, calculated from (C2 − C3)/C4 of glutamate or glutamine. Calculated values have no relation to control values at T0, and are not normalized to them. In the text there is a discussion of group H’s significantly greater PC/PDH for glutamine production. (B) Ratios of acetate/glucose consumption glutamate production, which at the end of the recovery period was significantly decreased in group D. Values for each time point are normalized to T0 control data. (CG) Metabolite quantifications for the last three time points, each measured relative to T0 control data. (C) Glutamate C2; (D) glutamine C2, which was always increased in the hypothermia group; (E) lactate C3; (F) glutamate C4, and (G) glutamine C4; (H) fractional 13C enrichment of lactate came from 1H data at 1.33 ppm, and was not normalized to control values. All data are presented as mean ± standard error values for three experiments. Significant differences, highlighted with asterisks, are defined with P < 0.0056, the Bonferroni-corrected upper limit 5% for type I errors.

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