T. Matsuoka et al., Repeated acute hypoxia temporarily attenuates the ventilatory respiratory response to hypoxia in conscious newborn rats, PEDIAT RES, 46(1), 1999, pp. 120-125
We asked whether repeated hypoxic exposures during the early neonatal perio
ds could affect the ventilatory control, such as the lung volume-dependent
ventilatory inhibition (HBR), pulmonary ventilation ((V) over dot E), and C
O2 production ((V) over dot CO2). 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 HER was triggered by lung inflation via ne
gative body surface pressure (10 cm H2O). Measurements of (V) over dot E an
d (V) over dot CO2 were done by plethysmography and the inflow-outflow CO2
difference, respectively. At 2 wk of age, (V) over dot E and (V) over dot C
O2 measurements were repeated by the barometric technique and the inflow-ou
tflow CO2 difference, respectively. Each conscious pup was breathing normox
ia (21% O-2) and then hypoxia (10% O-2). Results were as follows: 1) during
normoxia, HER was stronger and both (V) over dot E and (V) over dot CO2 we
re higher in H pups than in C pups; 2) during hypoxia, the HER of C was as
in normoxia, whereas that of ii was increased above the normoxic value; 3)
during hypoxia, C maintained (V) over dot E, whereas H decreased it; 4) in
hypoxia, (V) over dot CO2 was reduced significantly in both groups; 5) at 2
wk of age, (V) over dot E and (V) over dot CO2 did not differ between ii a
nd C during normoxia or in response to 10% hypoxia. We conclude that in rat
pups, repeated hypoxic episodes can modify the NBR and, at least temporari
ly, reduce the (V) over dot E response to hypoxia with a decrease in (V) ov
er dot CO2. The findings are in agreement with the view that repeated hypox
ic exposures in the neonatal. period could interfere with the development o
f respiratory control and could possibly be involved in the mechanisms of n
eonatal apnea or sudden infant death syndrome.