ObjectiveTo determine whether, during hemorrhagic shock, the effect of epinephrine on energy metabolism could be deleterious, by enhancing the oxygen requirement at a given level of oxygen delivery (DO2).DesignProspective, randomized, control trial.SettingExperimental laboratory.SubjectsTwo groups of seven mongrel dogs were studied. The epinephrine group received a continuous infusion of epinephrine (1 micro gram/min/kg) while the control group received saline.InterventionDogs were anesthetized with pentobarbital, and shock was produced by stepwise hemorrhage.Measurements and Main ResultsOxygen consumption (VO2) was continuously measured by the gas exchange technique, while DO2was independently calculated from cardiac output (measured by thermodilution) and blood oxygen content. A dual-lines regression fit was applied to the DO2vs. VO2plot. The intersection of the two regression lines defined the critical value of DO2. Values above critical DO2belonged to phase 1, while phase 2 occurred below critical DO2. In the control group, VO2was independent of DO2during phase 1; VO2was dependent on DO2during phase 2. In the epinephrine group, the expected increase in VO2(+19%) and DO2(+50%) occurred under normovolemic conditions. During hemorrhage, VO2immediately decreased, and the slope of phase 1 was significantly (p < .01) different from zero, and was significantly (p < .05) steeper than in the control group (0.025 +/- 0.005 vs. 0.005 +/- 0.010). However, the critical DO2(8.7 +/- 1.7 vs. 9.7 +/- 2.4 mL/min/kg), the critical VO2(5.6 +/- 0.5 vs. 5.5 +/- 0.9 mL/min/kg), and the slope of phase 2 (0.487 +/- 0.080 vs. 0.441 +/- 0.130) were not different from control values.ConclusionsThe administration of pharmacologic doses of epinephrine significantly increased VO2under normovolemic conditions due to the epinephrine-induced thermogenic effect. This effect progressively decreased during hemorrhage. The critical DO2and the relationship between DO2and VO2in the supply-dependent phase of shock were unaffected by epinephrine infusion. These results suggest that during hemorrhagic shock, epinephrine administration did not exert a detrimental effect on the relationship between DO2and VO2.(Crit Care Med 1995; 23:1272-1278)