Myocardial substrate utilization and hemodynamics were determined in dogs before and one hour and two hours after intravenous administration of sodium pentobarbital. Although total body O2 consumption decreased, along with arterial O2 concentration, there was no significant change in mean arterial pressure or cardiac output. Arterial free fatty acid (FFA) concentration and myocardial FFA remained the major energy source for the heart. Arterial glucose concentrations decreased significantly after pentobarbital, but myocardial uptake of glucose remained unchanged. Neither arterial lactic acid concentration nor myocardial lactate uptake was affected. Mocardial pyruvate uptake, by contrast, while remaining quantitatively the least of the contributors of energy measured, was more than double one hour after pentobarbital injection despite the fact that arterial pyruvate concentration did not increase. It is concluded that pentobarbital reduces the FFA utilization of both the whole animal and of its myocardium. The energy consumption of the whole animal is similarly diminished, whereas the energy used by myocardium is unchanged, other substrates evidently being substituted for FFA as energy sources.