Combined effects of intermittent hyperoxia and intermittent hypercapnic hypoxia on respiratory control in neonatal rats.

Highlights • Rats were exposed to alternating bouts of hypercapnic hypoxia and hyperoxia P0-P14. • Carotid body (CB) hypoxic responses were reduced but CB volumes were normal at P14. • Hypoxic ventilatory responses were normal despite weaker carotid body responses. • In contrast, sustained exposure to 30% O 2 blunted the HVR in neonatal rats. • Intermittent hypercapnic hypoxia reduced hyperoxia-induced plasticity in the HVR. Abstract Chronic exposure to intermittent hyperoxia causes abnormal carotid body development and attenuates the hypoxic ventilatory response (HVR) in neonatal rats. We hypothesized that concurrent exposure to intermittent hypercapnic hypoxia would influence this plasticity. Newborn rats were exposed to alternating bouts of hypercapnic hypoxia (10% O 2 /6% CO 2) and hyperoxia (30–40% O 2) (5 cycles h−1, 24 h d−1) through 13–14 days of age; the experiment was run twice, once in a background of 21% O 2 and once in a background of 30% O 2 (i.e., "relative hyperoxia"). Hyperoxia had only small effects on carotid body development when combined with intermittent hypercapnic hypoxia: the carotid chemoafferent response to hypoxia was reduced, but this did not affect the HVR. In contrast, sustained exposure to 30% O 2 reduced carotid chemoafferent activity and carotid body size which resulted in a blunted HVR. When given alone, chronic intermittent hypercapnic hypoxia increased carotid body size and reduced the hypercapnic ventilatory response but did not affect the HVR. Overall, it appears that intermittent hypercapnic hypoxia counteracted the effects of hyperoxia on the carotid body and prevented developmental plasticity of the HVR. [ABSTRACT FROM AUTHOR]