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Updated: Aug 19, 2026
A Piglet Model of Neonatal Hypoxic-Ischemic Encephalopathy
Published on: May 16, 2015
Habituation of arousal responses after intermittent hypercapnic hypoxia in piglets
Karen A Waters1, Kellie D Tinworth
1Department of Medicine, University of Sydney, Sydney NSW, Australia. kaw@mail.med.usyd.edu.au
Insights
Intermittent asphyxia can induce arousal deficits in infants, potentially explaining some infant deaths. This study shows that even short exposures to intermittent hypercapnic hypoxia can impair arousal responses.
Area of Science:
- Neonatal physiology
- Sleep medicine
- Respiratory control
Background:
- Infants with obstructive sleep apnea exhibit arousal deficits.
- These deficits are implicated in some infant deaths.
Purpose of the Study:
- To determine if intermittent asphyxia can induce arousal deficits during normal infant development.
- Investigate the impact of intermittent hypercapnic hypoxia on arousal responses.
Main Methods:
- Young piglets were exposed to intermittent hypercapnic hypoxia for four days.
- Arousal responses were measured and compared between control and experimental groups.
- Key outcomes included arousal latency and frequency during recovery.
Main Results:
- Arousal deficits were observed after initial exposures and worsened with successive exposures.
- Arousal latency increased significantly, indicating delayed responses.
- The frequency of arousals decreased by up to 90% after four days of exposure.
Conclusions:
- Intermittent asphyxia can acutely and chronically induce arousal deficits.
- These deficits occur even in the context of normal postnatal development.
- Findings suggest a mechanism linking asphyxia to impaired arousal in infants.
Rationale:
Clinical studies have demonstrated arousal deficits in infants suffering obstructive sleep apnea, and some infant deaths have been attributed to such an arousal deficit.
Objectives:
To evaluate whether arousal deficits can be induced by intermittent asphyxia during normal development.
Methods And Measurements:
Young piglets were exposed to intermittent hypercapnic hypoxia for 4 days from age 9.55 +/- 0.5 days. Arousal responses were compared between control animals and animals exposed to intermittent hypercapnic hypoxia. Outcome measures included time to arouse after onset of the respiratory stimulus and frequency of arousals during recovery.
Main Results:
Arousal deficits emerged after successive exposures to hypercapnic hypoxia on Day 1, and were exacerbated on Day 4, although after overnight recovery, the deficit only became evident during the second and subsequent episode of hypercapnic hypoxia. On Day 1, time to arouse increased from 16.9 +/- 7.1 seconds in the first epoch to 41.7 +/- 28.6 seconds in the fourth epoch (p = 0.004 between cycles, one-way analysis of variance). In the recovery periods after hypercapnic hypoxia, there were 64% fewer arousals than baseline on Day 1 and 90% fewer arousals on Day 4. Respiratory effort, measured by VT across 10 breaths before the arousal, increased from 25.7 +/- 7.6 on Day 1 to 29.1 +/- 6.8 ml/kg on Day 4 (p < 0.001, two-way analysis of variance, Day 4 vs. Day 1, respectively).
Conclusions:
These studies demonstrate that acute and chronic arousal deficits can be induced by intermittent asphyxia, on a background of otherwise normal postnatal development.
