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Effects on carotid chemoreceptor resetting of pulmonary ventilation in the fetal lamb in utero.

We tested the hypothesis that postnatal resetting of the carotid chemoreceptors is initiated by, and is dependent on, the rise in arterial PO2 (PaO2) which normally occurs after birth as air breathing is established. Previous studies had indicated that this resetting takes at least 24 h. We applied a technique for ventilation of the lungs of fetal sheep in utero to 3 groups of fetuses of 140-142 days gestational age: group 1 were exposed to normocapnic hyperoxia (mean PaO2 179.9 +/- 22.2 mmHg) for 27.4 +/- 0.9 h; group 2 were exposed to normocapnic hyperoxia (mean PaO2 229.4 +/- 77.5 mmHg) for 7.0 +/- 0.3 h; group 3 were ventilated for 21.6 +/- 3.3 h with a nitrogen/CO2 mixture to maintain PaO2 and PaCO2 within the normal fetal range. At the end of the ventilation period the fetuses were delivered by caesarean section, anaesthetized, paralysed and ventilation was continued. The responses of single or few fibre carotid chemoreceptor preparations to isocapnic hypoxia were then determined. To compare their response curves quantitatively, hyperbolic curves were fitted to the data. No significant differences between any of the groups were found in the vertical or the horizontal asymptotes. There was no difference in the slope of the hyperbolic line between group 2 and group 3. However, this slope was significantly greater for Group 1 than for either group 2 or group 3. Our results show that a period of hyperoxia of 24-31 h in utero, although not a similar period of normoxic ventilation, initiates the process of carotid chemoreceptor resetting.