Blockade of Electron Transport at the Onset of Reperfusion Decreases Cardiac Injury in Aged Hearts by Protecting the Inner Mitochondrial Membrane

<table>Measurement of mitochondrial calcium tolerance. Succinate (10 mM) was used to energize mitochondria. The upper panel (a) is an original tracing of calcium retention capacity (CRC). A calcium pulse (20 nmoles) was added each time. The release of calcium from mitochondria reflected opening of the permeability transition pore. The lower panel (b) shows that amobarbital treatment during reperfusion did not improve calcium tolerance in SSM and IFM compared to mitochondria from untreated hearts. (Mean ± SEM. <i>P</i> = NS versus untreated <svg height="10.9125" id="M31" style="vertical-align:-0.17555pt" version="1.1" viewbox="0 0 42.912498 10.9125" width="42.912498" xmlns="http://www.w3.org/2000/svg">
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Journal of Aging Research

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Figure 6

Figure 6: Blockade of Electron Transport at the Onset of Reperfusion Decreases Cardiac Injury in Aged Hearts by Protecting the Inner Mitochondrial Membrane 

Figure 6 | Blockade of Electron Transport at the Onset of Reperfusion Decreases Cardiac Injury in Aged Hearts by Protecting the Inner Mitochondrial Membrane 