Arterial oxygen consumption after hemorrhagic shock: the effect of beta-adrenergic agonist.

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 microliter/g/hr) when compared to oxygen consumption in the normal condition (2.52 +/- 0.22 microliter/g/hr). Application of the beta-agonist isoproterenol significantly increased oxygen consumption in the isolated femoral artery after hemorrhagic shock (2.66 +/- 0.20 microliter/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 microliter/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 beta-adrenergic receptors, and the phenomenon of diminished oxygen consumption after hemorrhagic shock probably occurs because of changes in beta-adrenergic receptors, causing the appearance of change in the mechanism of oxygen consumption.