In the mammalian foetus, the blood oxygen tension is low (PaO2 congruent to 25 Torr). The factors limiting the oxygen transfer from maternal into foetal blood are mainly the vascular arrangement and the distribution of blood flow within the placenta. The oxygen diffusion across the placenta in facilitated by a higher oxygen affinity in foetal than in maternal blood. During placental gas exchange the Bohr Effect acts in both the maternal and foetal blood to shift their oxyhaemoglobin dissociation curve so that the mean oxygen pressure gradient across the placental membrane is increased. The two main characteristics of foetal blood, a high oxygen capacity and a high oxygen affinity are well adapted to hypoxaemia since, together with a high cardiac output, they ensure an adequate oxygen supply to the foetal tissues. These characteristics of foetal blood disappear during the postnatal period in all the species thus far investigated. The change in the blood oxygen affinity which occurs in the foetus and the newborn have been attributed in some species to the presence of a foetal haemoglobin (HbF) which differs from the adult haemoglobin (HbA) either by an intrinsically higher oxygen affinity, independant of any intracellular cofactor, or by an impaired reactivity towards cofactors which alter haemoglobin oxygen affinity by directly interacting with the haemoglobin molecule (2,3 DPG, CO2). In those species in which HbF has not been shown to be structurally and functionally different from HbA, change in 2,3 DPG concentration can explain change in oxygen affinity.