Oxygen consumption of the rabbit femoral artery after hemorrhagic shock was studied. Hemorrhagic shock was initiated and maintained at 60 mm Hg of systolic blood pressure for 2 hours. A significant reduction in femoral artery oxygen consumption was observed after hemorrhagic shock (1.64 ± 0.14 μl/g/hr) when compared to oxygen consumption in the normal condition (2.52 ± 0.22 μl/g/hr). Application of the β-agonist isoproterenol significantly increased oxygen consumption in the isolated femoral artery after hemorrhagic shock (2.66 ± 0.20 μl/g/hr), but did not exceed the normal values recorded without stimulation. Also, isoproterenol significantly increased oxygen consumption in the femoral artery of nonhemorrhagic condition (4.84 ± 0.42 μl/g/hr). The increase in oxygen consumption conditioned by isoproterenol was significantly lower after hemorrhagic shock compared with values in the nonhemorrhagic state. The data suggest that oxygen consumption is regulated by β-adrenergic receptors, and the phenomenon of diminished oxygen consumption after hemorrhagic shock probably occurs because of changes in β-adrenergic receptors, causing the appearance of change in the mechanism of oxygen consumption.