This study was designed to test the hypothesis that the a2 adrenergic agonist, dexmedetomidine (DEX), decreases tissue oxygen demand thereby increasing tolerance to hypoxic insult. In 17 anaesthetized dogs, cardiac output was measured with thermodilution, blood flow through the inferior caval vein was determined using an electromagnetic flowmeter, and oxygen consumption was calculated by the Fick principle. The animals were divided into three groups: control group (n = 5), D3 and D30 groups (n = 6 for each group) treated with two doses of DEX (3 μg · kg-1 and 30 μg · kg-1, respectively) prior to aortic crossclamping. Upon crossclamping of the thoracic aorta, the cardiac index decreased in all three groups with the largest decrease in the D30 group, and the smallest decrease in the control group. Blood flow through the inferior vena cava decreased in all three groups of animals while blood flow through the superior caval vein increased in the control group, did not change in the D3 group, and decreased in the D30 group. Oxygen saturation in mixed venous blood increased in the control group, did not change in the D3 group and decreased in D30 group. Blood flow and oxygen uptake in the lower part of the body decreased in all groups. Oxygen consumption in the upper part of the body decreased equally in all three groups. Arterial lactate concentrations increased almost two-fold in the control group while it increased by only 30% in animals treated with DEX. A lesser increase in lactate concentrations and oxygen extraction in tissues below aortic crossclamping is consistent with the hypothesis that DEX decreases tissue oxygen requirement which might prove particularly useful in clinical situations where tissue hypoxia is expected. © 1992 Canadian Anesthesiologists.