Fetal breathing, sleep state and cardiovascular adaptations to anaemia in sheep.

1. In unanaesthetized fetal sheep (greater than 0.8 term) prolonged anaemia initially reduced the incidences of low‐voltage electrocortical activity, rapid eye movements and breathing activity; but the incidence of each returned to normal within 4‐7 h. 2. Anaemia induced a persistent rise in fetal heart rate and plasma concentrations of adrenaline, noradrenaline and cortisol. 3. After 16 h the fetal haematocrit was returned to normal. Isocapnic hypoxia induced less than 1 h later also inhibited eye and breathing activity. 4. After 1 h fetal arterial PO2 (Pa,O2) was returned to normal. This rise in O2 tension was associated with an elevation in the incidence of low‐voltage electrocortical activity, eye movements and breathing. Breathing movements also occurred during high‐voltage electrocortical activity. 5. It is concluded that the brain PO2 set‐point for hypoxic inhibition adapts rapidly to alterations in O2‐carrying capacity and is probably due to changes in the concentration and/or receptor affinity of a central neuromodulator. Secondly, a rise in brain PO2 at birth may contribute to the onset of continuous breathing.