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Thyroarytenoid muscle activity during hypoxia in awake lambs
1Centre Jeremy Rill, Département de Pédiatrie, Université de Sherbrooke, Quebec, Canada.
Journal of Applied Physiology (Bethesda, Md. : 1985)
|December 1, 1990
Summary
Hypoxia in young lambs does not cause laryngeal braking. Instead, recovery from hypoxia triggers active glottic adduction, prolonging expiration and controlling lung volume.
Area of Science:
- Neonatal Physiology
- Respiratory Control
- Laryngeal Reflexes
Background:
- Early-life hypoxia is thought to induce laryngeal braking of expiratory airflow.
- This braking is believed to involve glottic adductor muscle recruitment.
- The thyroarytenoid muscle plays a role in glottic adduction.
Purpose of the Study:
- To investigate thyroarytenoid muscle activity during hypoxia in newborn lambs.
- To determine if hypoxia triggers active glottic adduction and expiratory airflow braking.
- To examine the laryngeal response upon return to normoxia.
Main Methods:
- Electromyogram (EMG) activity of the thyroarytenoid muscle was recorded.
- Seven awake, nonsedated lambs (11-18 days old) were exposed to hypoxia (inspired O2 fraction of 0.08).
- Breathing was monitored using a face mask and pneumotachograph; flow-volume curves were analyzed.
Main Results:
- The thyroarytenoid muscle was largely inactive during baseline breathing.
- No thyroarytenoid muscle recruitment or expiratory airflow braking was observed during hypoxia.
- Marked thyroarytenoid muscle activity and delayed expiration occurred upon return to room air.
Conclusions:
- Active expiratory glottic adduction is absent during hypoxia in awake, 11- to 18-day-old lambs.
- Recovery from hypoxia induces active glottic adduction and prolonged expiration.
- This post-hypoxic response helps control end-expiratory lung volume.