In healthy subjects, when oxygen transport is gradually decreased, oxygen consumption is maintained as tissue oxygen extraction is increased. When delivery is decreased further, there is a critical level below which tissue extraction cannot increase in proportion to the reduced delivery, and oxygen consumption falls. Blood lactate levels then rise, a sign of tissue hypoxia, despite further increases in oxygen extraction as delivery drops below this critical level. There are two major mechanisms which tend to prevent tissue hypoxia in case of reduced oxygen delivery: regional redistribution of blood flow and an increase in the number of perfused capillaries. This possibility of regulating blood flow distribution may be lost during disseminated intravascular coagulation, alpha-adrenergic receptor blockade, hypothermia, arteriovenous shunting. All these alterations have been reported as occurring in sepsis. An abnormal dependency on oxygen supply is observed during bacteriaemia or endotoxinaemia. This is secondary to a reduced ability, at the whole body level, to extract oxygen from a limited supply. The inability to increase oxygen extraction is related to a maldistribution of the cardiac output, with "stealing" of blood, i.e. overperfusion of some organs (skeletal muscle) rather than those where perfusion is rapidly compromised (small intestine). Endotoxin also reduces the efficacy of oxygen extraction within the isolated intestinal segment, whereas that within other organs is preserved. These observations are similar to findings in patients with sepsis who seem to have both an increased demand in oxygen, and a reduced ability to extract it at the tissue level.