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Published on: November 2, 2015
Respiratory and metabolic responses to early postnatal chronic intermittent hypoxia and sustained hypoxia in the
Stephen R Reeves1, David Gozal
1Department of Pediatrics, Kosair Children's Hospital Research Institute, University of Louisville School of Medicine, Louisville, Kentucky 40202, USA.
Insights
Postnatal intermittent hypoxia (IH) and sustained hypoxia (SH) alter breathing patterns in developing rats. IH causes higher resting ventilation, while both IH and SH modify the hypoxic ventilatory response (HVR) differently.
Area of Science:
- Physiology
- Developmental Biology
- Respiratory Medicine
Background:
- Sustained hypoxia (SH) differentially affects the hypoxic ventilatory response (HVR) in adult and developing mammals.
- Postnatal intermittent hypoxia (IH), a common clinical condition, may significantly alter ventilatory patterning during development.
Purpose of the Study:
- To investigate the effects of postnatal intermittent hypoxia (IH) on ventilatory patterning and HVR in developing rats.
- To compare the effects of IH with sustained hypoxia (SH) on respiratory development.
Main Methods:
- Sprague-Dawley rat pups were exposed to normoxia, SH (10% O2), or IH (alternating room air and 10% O2) from postnatal day 1 to 30.
- Whole-body plethysmography was used to assess HVR in unrestrained pups at 5, 10, 15, and 30 days of age.
Main Results:
- IH pups exhibited significantly higher normoxic ventilation (VE) at all ages compared to controls.
- SH exposure led to increased VE only after 10 days.
- Both SH and IH altered peak HVR (pHVR) and hypoxic ventilatory decline (HVD), with distinct ventilatory strategies observed between the two conditions.
Conclusions:
- Both IH and SH significantly modify normal ventilatory patterning in developing rats.
- Postnatal IH and SH induce altered HVR but employ different ventilatory strategies to achieve these responses.
Abstract:
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 < 0.001 versus control; n = 12 per group), which was not observed in SH animals until 10 d of exposure (p < 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.
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