1. In seven unanaesthetized fetal sheep (> 80% term), isocapnic hypoxi
a (arterial partial pressure of O-2, P-a,P-O2, similar to 15 mmHg) was
induced for 1 h by lowering maternal inspired P-O2. Fetal hypoxia was
also produced during intra-arterial administration of the adenosine r
eceptor antagonist 8-(p-sulphophenyl)-theophylline (8-SPT). The fetal
8-SPT infusion was begun just prior to hypoxia and was stopped when fe
tal P-a,P-O2 was returned to normal. 2. Hypoxia induced a progressive
fetal acidosis, a rise in mean arterial pressure, a transient fall in
heart rate and a decrease in breathing movements. 8-SPT signivicantly
reduced the metabolic acidosis and abolished the hypertension and brad
ycardia without altering hypoxic inhibition of fetal breathing. Admini
stration of the vehicle for 8-SPT during hypoxia did not significantly
affect the normal fetal metabolic and cardiovascular responses to acu
te O-2 deprivation. 3. It is concluded that adenosine mediates the fet
al bradycardia and hypertension produced by hypoxia, indicating that a
denosine modulates fetal autonomic responses to acute oxygen deficienc
y Secondly, adenosine contributes to fetal metabolic acidaemia, sugges
ting that adenosine also modulates fetal glycolytic responses to hypox
ia.