A description is given of the effect of hypercapnic acidaemia and hypocapnic alkalaemia on scalp tissue PO2 as measured with a subcutaneous needle-electrode and a transcutaneous electrode in 6 fetal lambs. The experiments were carried out under general anaesthesia with the fetus kept in utero. Hypocapnia was induced by hyperventilating the ewe and hypercapnia was achieved by administering extra CO2 to the ewe. Fetal carotid arterial, subcutaneous and transcutaneous PO2 were continuously recorded, and fetal and maternal arterial pH and arterial PCO2 were determined from blood samples taken at short intervals. In each experiment the H+ Bohr factor of fetal and maternal blood was measured. During hypocapnic alkalaemia, there was a fall in all fetal PO2 levels, whereas a marked rise was observed during hypercapnic acidaemia. The variations in fetal PO2 observed in vivo even exceeded the variations due to the H+ Bohr effect (measured in vitro). This was due to small variations in fetal carotid arterial oxygen saturation, which tended to fall during hypocapnic alkalaemia and to rise during hypercapnic acidaemia. The results of these findings strongly suggest that tissue PO2, as measured with the subcutaneous and transcutaneous electrodes, is dependent on the H+ Bohr effect. This adds to the uncertainty as to the value of subcutaneous and transcutaneous PO2 monitoring during labour as an early warning system for impending fetal asphyxia.