Repeated acute hypoxia temporarily attenuates the ventilatory respiratory response to hypoxia in conscious newborn rats.

We asked whether repeated hypoxic exposures during the early neonatal periods could affect the ventilatory control, such as the lung volume-dependent ventilatory inhibition (HBR), pulmonary ventilation (VE), and CO 2 production (VCO 2 ). Within each litter of rats, one group of pups (experimental group H) was exposed to 6% O 2 (30-min duration twice a day from postnatal d 1 to 4). The other group (control group C) was exposed to air. At 5 d after birth, the HBR was triggered by lung inflation via negative body surface pressure (10 cm H 2 O). Measurements of VE and VCO 2 were done by plethysmography and the inflow-outflow CO 2 difference, respectively. At 2 wk of age, VE and VCO 2 measurements were repeated by the barometric technique and the inflow-outflow CO 2 difference, respectively. Each conscious pup was breathing normoxia (21% O 2 ) and then hypoxia (10% O 2 ). Results were as follows: 1) during normoxia, HBR was stronger and both VE and VCO 2 were higher in H pups than in C pups; 2) during hypoxia, the HBR of C was as in normoxia, whereas that of H was increased above the normoxic value; 3) during hypoxia, C maintained VE, whereas H decreased it; 4) in hypoxia, VCO 2 was reduced significantly in both groups; 5) at 2 wk of age, VE and VCO 2 did not differ between H and C during normoxia or in response to 10% hypoxia. We conclude that in rat pups, repeated hypoxic episodes can modify the HBR and, at least temporarily, reduce the VE response to hypoxia with a decrease in VCO 2 . The findings are in agreement with the view that repeated hypoxic exposures in the neonatal period could interfere with the development of respiratory control and could possibly be involved in the mechanisms of neonatal apnea or sudden infant death syndrome.