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Exposure to sustained hypoxia (SH) differentially modifies the hypoxic ventilatory response (HVR) in adults and developing rats. We examined the possibility that postnatal intermittent hypoxia (IH), a more prevalent clinical condition than SH, may lead to significant modifications of ventilatory patterning during development. Sprague-Dawley rat pups were exposed as of the d 1 of life to either SH (10% O2) or IH [alternating room air (RA) and 10% O2 every 90 s] for up to 30 d; controls were exposed to normoxia. HVR (10% O2 for 20 min) was assessed in unrestrained pups at 5, 10, 15, and 30 d of age using whole-body plethysmography. IH pups displayed higher normoxic ventilation (VE) at all ages (p &lt; 0.001 versus control; n = 12 per group), which was not observed in SH animals until 10 d of exposure (p &lt; 0.001 versus control; n = 12 per group). Furthermore, both SH and IH modified properties of peak HVR (pHVR), as well as those of the ensuing hypoxic ventilatory decline (HVD); however, the ventilatory strategies adopted after SH and IH greatly differed. We conclude that both postnatal IH and SH modify normal ventilatory patterning and induce altered HVR, but differ in the ventilatory strategies adopted to mount HVR responses.

Respiratory and Metabolic Responses to Early Postnatal Chronic Intermittent Hypoxia and Sustained Hypoxia in the Developing Rat