Carotid body O 2 sensitivity during chronic hyperoxia and after recovery in normoxia

Developmental hyperoxia attenuates the hypoxic ventilatory response (HVR), an effect which persists into adulthood despite return to normoxia. Part of this impairment is due to carotid body hypoplasia and loss of afferent neurons, but part may be due to impaired responses of the surviving cells. To investigate chemoreceptor function during hyperoxia and after return to normoxia, rat pups were exposed to 60% O 2 from birth through P7 and then returned to normoxia until P14. Single‐unit responses to hypoxia were recorded in vitro at ages P1‐P7 (hyperoxia) and at P10 and P14 (recovery). Hyperoxia reduced chemoreceptor responses during acute hypoxia by 4–5 days hyperoxia treatment, consistent with an earlier study (Donnelly et al., Respir. Physiol. Neurobiol. 68:189–197, 2009). Interestingly, these responses recovered to control levels within one week of return to normoxia. These data indicate that carotid chemoreceptor responses to hypoxia are labile during the postnatal period. Moreover, these data do not support a role for reduced O 2 sensitivity of surviving cells in long‐lasting reduction of the HVR after developmental hyperoxia. Supported by NIH grants HL‐083972, RR‐016463 (Maine INBRE) and HL‐073500.