Abstract
1. Newborn rats and their mothers were exposed from birth in a normobaric environmental chamber to an inspired O2 fraction (FI, O2) of 0.13-0.15 for 5-10 weeks. 2. The respiratory response to reducing FI, O2 to 0.12 or 0.08 for 6 min was measured in the conscious chronically hypoxic rat pups on post-natal days 5 and 14 and again at 5-10 weeks of age. On days 5 and 14 the responses were compared to those of normoxic control pups also exposed acutely to an FI, O2 of 0.12 or 0.08. 3. No significant respiratory response to the acute reduction in FI, O2 was found in the chronically hypoxic pups on post-natal days 5 and 14, whereas the normoxic pups showed a ''biphasic'' respiratory response on day 5 and a sustained (''adult'') response on day 14. A ''biphasic'' respiratory response to an FI, O2 of 0.08, but not to an FI, O2 of 0.12, was seen in the chronically hypoxic pups at 5-10 weeks of age. 4. At 5-10 weeks recordings from the carotid sinus nerve were made in anaesthetized, paralysed and artificially ventilated rats. The isocapnic hypoxic response curves of chronically hypoxic rats were not significantly different from those of age-matched normoxic rats. 5. Our results suggest that limiting the rise in arterial O2 pressure which usually occurs at birth alters the ventilatory response to acute hypoxia by post-natal day 5 and this alteration is still evident at 5-10 weeks of age. 6. The results are discussed in terms of two opposing components which determine ventilation (.ovrhdot.VE) during acute hypoxia in the neonate: (a) the peripheral arterial chemoreceptors which stimulate .ovrhdot.VE and (b) a central nervous component which inhibits .ovrhdot.VE. Chronic hypoxia from birth appears to reduce drastically the rate of disappearance of the central nervous component, delaying the appearance of the ''adult'' response to acute hypoxia.