Abstract
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.