Developmental hyperoxia attenuates the hypoxic ventilatory response in Japanese quail (Coturnix japonica).

Early life experiences can influence development of the respiratory control system. We hypothesized that chronic hyperoxia (60% O(2)) during development would attenuate the hypoxic ventilatory response (HVR) of Japanese quail (Coturnix japonica), similar to the effects of developmental hyperoxia in mammals. Quail were exposed to hyperoxia during prenatal development, during postnatal development, or during both prenatal and postnatal development (for approximately 2 or 4 weeks). HVR (11% O(2)) was subsequently assessed in adults (>6 weeks old) via barometric plethysmography and compared to quail raised in normoxia (i.e., control). The HVR of quail exposed to hyperoxia both prenatally and postnatally was reduced 50-60% compared to control quail whereas postnatally exposed quail exhibited normal HVR. The effects of prenatal hyperoxia on HVR were equivocal and depended on how HVR was expressed. We conclude that developmental exposure to 60% O(2) attenuates the HVR in quail and that the critical period for this plasticity encompasses the late prenatal and early postnatal periods.

Hypoxic ventilatory responses in rats after hypercapnic hyperoxia and intermittent hyperoxia.

Perinatal hyperoxia attenuates the adult hypoxic ventilatory response in rats. Hyperoxia might elicit this plasticity by inhibiting chemoreceptor activity during early life. Thus, we hypothesized that stimulating chemoreceptors with CO(2) during hyperoxia or interrupting hyperoxia with periods of normoxia would reduce the effects of hyperoxia on the hypoxic ventilatory response. Rats were born and raised in 60% O(2) for the first two postnatal weeks. Two groups were simultaneously exposed to either sustained hypercapnia (5% CO(2)) or intermittent hypercapnia (alternating 1-h exposures to 0 and 7.5% CO(2)) while another group was exposed to only intermittent hyperoxia (alternating 1-h exposures to 21 and 60% O(2)). Hypoxic ventilatory responses were assessed at 6-10 weeks of age by whole-body plethysmography. Rats exposed to intermittent hypercapnia during hyperoxia or to intermittent hyperoxia exhibited greater increases in ventilation-to-metabolism ratio ( VE/VO2 ) in response to 12.5% O(2) than rats exposed to hyperoxia alone (both P<0.05), although responses were generally less than those of normoxia-reared controls; a similar trend was observed for rats exposed to sustained hypercapnia during hyperoxia (P=0.053). These data suggest that activity-dependent mechanisms contribute to hyperoxia-induced developmental plasticity, although contributions from additional mechanisms cannot be excluded.