Background: Fatty acid (FA) metabolism is suppressed under conditions of cardioplegic arrest, but the mechanism behind this effect is unknown. We hypothesized that alterations in redox state and oxygen demand control myocardial FA utilization during potassium arrest.
Methods: Rat hearts were perfused with Krebs-Heinseleit buffer containing physiologic concentrations of FAs, ketones, and carbohydrates with unique (13)Carbon labeling patterns. Cytosolic and mitochondrial redox states were altered by manipulating the lactate/pyruvate and ketone redox couples, respectively. Myocardial oxygen consumption was increased by adding the mitochondrial uncoupler 2,4-dinitrophenol to the perfusate. Experiments were conducted under conditions of normokalemic perfusion and potassium cardioplegia (PC). Substrate oxidation rates were derived from (13)Carbon isotopomer data and myocardial oxygen consumption.
Results: Continuous perfusion under conditions of potassium arrest dramatically reduced fatty acid oxidation. Both the addition of 2,4-dinitrophenol and alteration of mitochondrial redox state significantly increased FA oxidation during PC. In contrast to normokalemic perfusion, altering cytosolic redox state during PC did not change FA oxidation.
Conclusions: These data suggest that mitochondrial redox state and oxygen demand are important determinants of myocardial FA oxidation during potassium arrest. FA oxidation appears to be regulated by different factors during PC than normokalemic perfusion.
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