Cardiorespiratory effects of chronic hyperoxia in neonatal rats

Abstract

Rats reared in hyperoxia (60% O2) from birth exhibit abnormal respiratory control: normoxic ventilation is reduced at 4 and 7 d of age (i.e., P4 and P7), but not at P14, and the hypoxic ventilatory response (HVR) is blunted at P7 and P14, but not at P4 (Bavis et al. J Appl Physiol 109: 796–803, 2010). To determine whether these respiratory deficits impair tissue O2 delivery, arterial O2 saturation (SpO2) and heart rate were measured by pulse oximetry at P4 and P14 for rats reared in 60% O2 (Hyperoxia) or 21% O2 (Control). At P4, Hyperoxia rats had lower SpO2 (93.0±1.3 vs. 98.8±0.2%; mean±SEM) and lower heart rates (332±10 vs. 380±9 bpm) while in normoxia than Controls. SpO2 was also lower in Hyperoxia rats at P14, but to a lesser extent (97.0±0.4 vs. 98.7±0.1%); heart rate was not different from Controls at P14. When exposed to hypoxia (12% O2), the drop in SpO2 was greater in Hyperoxia rats than Controls; however, this difference was more pronounced at P14 (ΔSpO2 = −42±2 vs. −24±2% in Controls), consistent with the blunted HVR of Hyperoxia rats at this age. Hyperoxia rats also had lower hematocrits at P4 and P14 and smaller hearts at P4. Therefore, Hyperoxia rats do not appear to compensate for low SpO2 and heart rate by increasing blood O2 capacity or stroke volume. Together, these data suggest that tissue O2 delivery is compromised during both normoxia and acute hypoxia in neonatal rats reared in hyperoxia. Supported by NIH grant HL‐083972.