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. 2011 Oct 4;302(2):E163–E172. doi: 10.1152/ajpendo.00443.2011

Fig. 8.

Fig. 8.

Peri-infarct mitochondria. A: peri-infarct permeabilized cardiac fiber basal oxygen consumption supported by glutamate and malate (V0), maximal oxygen consumption supported by glutamate and malate through complex I (Vmax-CI), and maximal convergent oxygen consumption supported by glutamate, malate, and succinate (Vmax-CI + CII). B: respiratory control ratio (RCR; defined as Vmax-CI/V0) and succinate control ratio (SCR; defined as Vmax-CI + CII/Vmax-CI); n = 8 mice/group. C: mitochondrial oxidative phosphorylation (OXPHOS) complexes, uncoupling protein 3 (UCP3), adenine nucleotide translocase (ANT), and glutathione peroxidase (GPx) from the peri-infarct region, as determined by immunoblotting. D: representative immunoblotting of OXPHOS complexes, UCP3, ANT, GPx, and voltage-dependent anion channel (VDAC). Protein levels were normalized to VDAC content and are relative to the SHAM group; n = 6 mice/group. Of note, the order presentation of the groups in D is different from the order presentation of the groups in C. E: citrate synthase (CS) activity (mmol·min−1·mg protein−1). F: relative CI + CIII activity (mol·min−1·mg protein) normalized to CS; n = 6–8 mice/group. Data are means ± SE. *P < 0.05 vs. SHAM; †P < 0.05 vs. MI + PBS.