Abstract

Hypoxia sustained during the prenatal period lowers the ventilatory (V˙(E)) response to hypoxia of the newborn. This phenomenon probably results from a disturbance in the normal development of the peripheral chemoreceptors, as shown to be the case postnatally after sustained period of low or high oxygen. To test the possibility that prolonged prenatal hyperoxia may have a similar effect, the breathing pattern and the V˙(E) responses to hypoxia or hypercapnia were measured by a modification of the barometric technique in 1-day old chicken hatchlings exposed to 40% O2 or 60% O2 (N=16 each) during the last week of incubation (hatching included), and in controls incubated in normoxia (N=16). During air breathing and moderate hypoxia (15% O2), neither group differed from controls. However, the V˙(E) response to 10% O2 was reduced to less than half normal in both groups of prenatal-hyperoxia hatchlings. The hypoxic drop in oxygen consumption V˙(O2) was more marked than in controls, which probably helped to limit the degree of hypoxemia and to sustain the hyperventilation (increase in V˙(E)-V˙(O2) ratio). The V˙(E) response to hypercapnia was almost normal, suggesting that there was no mechanical limitation on V˙(E). The degree of blunting in the V˙(E) response to hypoxia was very similar to that previously measured in hatchlings exposed to hypoxia during the last week of incubation. The results support to the view that sustained changes in oxygenation during the prenatal period reduce the newborn's V˙(E) response to hypoxia probably because of a major dysfunction of the carotid bodies.

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