Adrenergic agents (AAs) have been used in critically ill patients to increase oxygen delivery (DO2). Associated parallel increases in oxygen consumption (VO2) have been noted and are thought to represent improved tissue oxygen utilization at supraphysiologic levels of DO2. We hypothesize that the increase in VO2 associated with the use of AAs in septic animals is secondary to direct, obligate, metabolic effects of the agents themselves. In this study, mongrel dogs were anesthetised, paralyzed, and had minimum temperature maintained on a warming blanket. Pulmonary and systemic hemodynamics were monitored. DO2 was calculated, while VO2 was measured directly with a metabolic cart. All dogs were given an Escherichia coli challenge and a colloid fluid resuscitation. Two hours after the onset of endotoxemia, baseline values were obtained, followed by four progressively larger doses of saline, dobutamine, or dopamine. At each dose there was a 40-min stabilization period and a 20-min measurement of hemodynamics and VO2. Data were analyzed using analysis of variance with a Scheffe's S test. P values of < 0.05 were considered significant. The control group slowly decreased VO2 during the 6-hr experiment to 73% of baseline. Dobutamine increased VO2 to 119% of baseline (31% above control) and dopamine to 111% of baseline (28% over control). We conclude that adrenergic agents cause a significant increase in whole body VO2 at moderate doses in septic dogs. It is likely, therefore, that the "pathologic" relationship between VO2 and DO2 described in critically ill patients is partially due to the direct metabolic effects of AAs.