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Laboratory and Animal Investigations |

Chronic Intermittent Asphyxia Impairs Rat Upper Airway Muscle Responses to Acute Hypoxia and Asphyxia*

Ken D. O’Halloran, PhD; Michelle McGuire, PhD; Turlough O’Hare, MSc; Aidan Bradford, PhD
Author and Funding Information

*From the Department of Human Anatomy and Physiology (Dr. O’Halloran), University College Dublin, Dublin, Ireland; and the Department of Physiology (Drs. McGuire and Bradford, and Mr. O’Hare), Royal College of Surgeons in Ireland, Dublin, Ireland.

Correspondence to: Ken D. O’Halloran, PhD, Department of Human Anatomy and Physiology, University College Dublin, Earlsfort Terrace, Dublin 2, Ireland; e-mail: ken.ohalloran@ucd.ie



Chest. 2002;122(1):269-275. doi:10.1378/chest.122.1.269
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Background: Obstructive sleep apnea (OSA) is a major clinical disorder that is characterized by multiple episodes of upper airway obstruction due to the failure of the upper airway dilator muscles to maintain upper airway patency. This results in chronic intermittent asphyxia (CIA) due to repetitive apneas, but very little is known about the effects of CIA on upper airway muscle function.

Objective: To test the hypothesis that CIA affects upper airway muscle activity and electromyogram (EMG) responses to acute hypoxia and asphyxia.

Design: Record upper airway EMG responses to acute hypoxia and asphyxia in control and CIA-treated rats.

Setting: Department of Physiology, Royal College of Surgeons in Ireland, Dublin, Ireland.

Measurements: Sternohyoid (SH) muscle and diaphragm (DIA) muscle EMG activities were recorded in both groups during normoxia, hypoxia (7.5% O2 in N2), and asphyxia (7.5% O2 and 3% CO2) under pentobarbitone anesthesia.

Results: Baseline SH EMG activity was significantly elevated in the CIA-treated rats compared to the controls, whereas DIA EMG activity was similar in the two groups. In addition, CIA significantly reduced SH EMG but not DIA EMG responses to acute hypoxia and asphyxia.

Conclusions: The elevated upper airway muscle activity associated with OSA in humans during wakefulness is due at least in part to CIA. We propose that a reduction in the response of upper airway dilator muscles to acute asphyxia following upper airway obstruction is likely to cause further asphyxic insult, leading to a vicious feed-forward cycle exacerbating the condition. Our results suggest that CIA contributes to the pathophysiology of sleep-disordered breathing.

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