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Fig. 5 | Journal of Translational Medicine

Fig. 5

From: Trauma/hemorrhagic shock instigates aberrant metabolic flux through glycolytic pathways, as revealed by preliminary 13C-glucose labeling metabolomics

Fig. 5

Blood from trauma/hemorrhagic shock rats (laparotomy with bowel crush, with hemorrhagic shock to MAP < 30) was withdrawn before injection (baseline B) of labeled 13C-glucose (iLC) preceding hemorrhagic shock. Blood was then collected at 5, 10, 15 and 35 min after iLC. Metabolites of glycolysis and Krebs cycles were monitored, as they have been previously shown to increase in plasma after trauma/hemorrhagic shock [14]. In left, the total levels of the metabolite (integrated peak areas—arbitrary units) are indicated through stacked bar graphs, including the unlabeled parent (blue M + 0) and heavy isotopologues (either M + 2, M + 3 or M + 4 depending on the expected labeling pattern from catabolism of 13C-glucose—a schematic overview is provided in the upper right corner). In the right hand panels, only heavy isotopologues (M + 2 = red, M + 3 = yellow, M + 4 = orange, M + 6 = green) are shown. As soon as 10 min after iLC, hemorrhagic shock induced accumulation of lactate and unlabeled glucose (indicative of ongoing gluconeogenesis) and late Krebs cycle intermediates (succinate, fumarate, malate), increased levels of glutamate and totally unlabeled urate, polyamines (spermidine), glutathione (either reduced—GSH and oxidized—GSSG), mannitol and citramalate.

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