Myocardial Oxygen Consumption and Mitochondrial Membrane Potential in Post-Ischemic Myocardium
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概要
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Myocardial oxygen consumption (MVO<SUB>2</SUB>) may be disproportionately high relative to contractile function in post-ischemic, reperfused myocardium. This study investigated the mechanism of dissociation between MVO<SUB>2</SUB> and contractile function in post-ischemic, reperfused myocardium using isolated rat hearts. Mitochondrial dysfunction secondary to increased calcium uptake has been implicated as an important mediator of reperfusion injury in the heart. In post-ischemic, isovolumic, antegrade-perfused rat hearts, MVO<SUB>2</SUB> rate and contractile function were studied in relation to mitochondrial function. Left ventricular pressure, coronary blood flow, and MVO<SUB>2</SUB> were determined. Mitochondrial respiration and membrane potential were measured by polarography and flow cytometry. To examine the role of mitochondrial calcium uptake in ischemic reperfusion injury, isolated rat hearts perfused with ruthenium red (an inhibitor of calcium uptake) were compared to control perfused hearts. Hearts were subjected to 60 minutes of no-flow ischemia, followed by 60 minutes of reperfusion. At 15 minutes after the onset of reperfusion, there was poor recovery of left ventricular pressure to 54% of the control level, but MVO<SUB>2</SUB> increased to 149% of the control. Addition of 2.5μM ruthenium red to the perfusate resulted in a decrease in MVO<SUB>2</SUB>. The oxygen consumption rate in state 3 mitochondria decreased similarly following reperfusion both in control and in ruthenium red hearts. The mitochondrial membrane potential was reduced to 89% (logarithmic scale) after 15 minutes of reperfusion. This data suggests that the dissociation between MVO<SUB>2</SUB> and contractile function following early reperfusion is partly caused by the repair of intracellular damage resulting from reduction of the mitochondrial membrane potential.
- 昭和大学・昭和医学会の論文
昭和大学・昭和医学会 | 論文
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