Effects of Perinatal Hyperoxia on Breathing

Abstract Air‐breathing animals do not experience hyperoxia (inspired O 2 > 21%) in nature, but preterm and full‐term infants often experience hyperoxia/hyperoxemia in clinical settings. This article focuses on the effects of normobaric hyperoxia during the perinatal period on breathing in humans and other mammals, with an emphasis on the neural control of breathing during hyperoxia, after return to normoxia, and in response to subsequent hypoxic and hypercapnic challenges. Acute hyperoxia typically evokes an immediate ventilatory depression that is often, but not always, followed by hyperpnea. The hypoxic ventilatory response (HVR) is enhanced by brief periods of hyperoxia in adult mammals, but the limited data available suggest that this may not be the case for newborns. Chronic exposure to mild‐to‐moderate levels of hyperoxia (e.g., 30–60% O 2 for several days to a few weeks) elicits several changes in breathing in nonhuman animals, some of which are unique to perinatal exposures (i.e., developmental plasticity). Examples of this developmental plasticity include hypoventilation after return to normoxia and long‐lasting attenuation of the HVR. Although both peripheral and CNS mechanisms are implicated in hyperoxia‐induced plasticity, it is particularly clear that perinatal hyperoxia affects carotid body development. Some of these effects may be transient (e.g., decreased O 2 sensitivity of carotid body glomus cells) while others may be permanent (e.g., carotid body hypoplasia, loss of chemoafferent neurons). Whether the hyperoxic exposures routinely experienced by human infants in clinical settings are sufficient to alter respiratory control development remains an open question and requires further research. © 2020 American Physiological Society. Compr Physiol 10:597‐636, 2020.