Oxidative metabolism of myocardium as influenced by fatty acids and epinephrine

Abstract

Oxygen consumption of the K-arrested isolated rat heart was significantly increased by [beta]-hydroxy-butyrate and by octanoate. Palmitate, octanoate, and [beta]-hydroxybutyrate, all of which increase qO2 [respiratory quotient] in this preparation, also increased intracellular citrate levels. Glucose caused neither of these effects. Fluoroacetate increased citrate levels without increas-ing qO2. Oligomycin decreased qO2, caused arrest, and diminished ATP concentrations, suggesting that oligomycin inhibits oxidative phosphorylation in the intact tissue as it does in isolated mitochondria. Neither the basal qO2 of the K-arrested heart nor the increase due to octanoate was affected by oligomycin. These results suggest that there are pathways of respiration in the intact tissue not tightly coupled to ATP formation and that the increase of qO2 caused by fatty acids may involve such pathways. The epinephrine-induced increase in O2 consumption of the beating heart was accompanied by a highly significant increase in intracellular free fatty acid concentration. The possible relationship of this to the metabolic component of the epinephrine effect on myocardium is discussed.