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Exacerbation of Obstructive Sleep Apnea by Oral Indomethacin

Keith R. Burgess, PhD; Jue-Lin Fan, BSc; Karen Peebles, MSc; Kate Thomas, BSc; Sam Lucas, PhD; Rebecca Lucas, BSc; Andrew Dawson, BSc; Marianne Swart, BSc; Kelly Shepherd, PhD; Phil Ainslie, PhD
Author and Funding Information

Correspondence to: Keith R. Burgess, PhD, Peninsula Sleep Laboratory, Ste 3, Level 2, 1/49 Frenchs Forest Rd, Frenchs Forest, NSW, Australia 2086; e-mail: krburgess@optusnet.com.au


Funding/Support: This study was supported by the Peninsula Health Care Pty Ltd (funding for travel for three technicians and equipment purchase), Otago Medical Research (funding for equipment purchases), Air Liquide Pty Ltd (special gas mixtures), and AD Instruments (loan equipment for measurement of ventilatory responses and cerebral blood flow).

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestpubs.org/site/misc/reprints.xhtml).


© 2010 American College of Chest Physicians


Chest. 2010;137(3):707-710. doi:10.1378/chest.09-1329
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Patients with obstructive sleep apnea (OSA) are predisposed to instability in central ventilatory control during sleep. Increased instability, as reflected in an enhanced expired volume in per unit time loop gain, has been associated with a greater predisposition to upper airway collapse. Here, in an otherwise healthy patient with untreated mild OSA, we describe the further exacerbation of OSA after oral indomethacin administration. The subject was a control subject in part of a study to investigate the effects of altering cerebral blood flow (CBF) on ventilatory responses and sleep. He was administered either placebo or 100 mg of indomethacin orally with 20 mL of antacid 2.5 h before sleep on different days. He was studied overnight by polysomnography, arterial blood gases, and transcranial Doppler ultrasound. Administration of 100 mg of oral indomethacin prior to sleep resulted in an almost doubling of the apnea-hypopnea index (14 to 24/h), compared with placebo. This was due to an increase in apneas, rather than hypopneas. Following the indomethacin, changes in arterial blood gases were unremarkable, but both CBF as indexed using transcranial Doppler ultrasound and CBF reactivity to a steady-state change in CO2 (CBF-CO2) reactivity were reduced, and the ventilatory response to CO2 was elevated. CBF was also further reduced during nonrapid eye movement sleep following the indomethacin when compared with the control night. Indomethacin-induced reductions in CBF and CBF-CO2 reactivity and related increases in ventilatory instability may lead to a greater predisposition to upper airway collapse and related apnea; these factors may partly explain the exacerbation of OSA.

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