HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Free Full Text (PDF) Free All Versions of this Article: 103/2/578    most recent 00017.2007v1 Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (1) Citing Articles via Google Scholar Google Scholar Articles by Smith, C. A. Articles by Dempsey, J. A. Search for Related Content PubMed PubMed Citation Articles by Smith, C. A. Articles by Dempsey, J. A.

The apneic threshold during non-REM sleep in dogs: sensitivity of carotid body vs. central chemoreceptors

¹John Rankin Laboratory of Pulmonary Medicine and Department of Population Health Sciences, University of Wisconsin, Madison, Wisconsin; and ²Laboratoire de Physiologie, Faculté de Médecine de Nancy, Université Henri Poincaré, Nancy France

Submitted 4 January 2007 ; accepted in final form 8 May 2007

The relative importance of peripheral vs. central chemoreceptors in causing apnea/unstable breathing during sleep is unresolved. This has never been tested in an unanesthetized preparation with intact carotid bodies. We studied three unanesthetized dogs during normal sleep in a preparation in which intact carotid body chemoreceptors could be reversibly isolated from the systemic circulation and perfused. Apneic thresholds and the CO₂ reserve (end-tidal PCO₂ eupneic – end-tidal PCO₂ apneic threshold) were determined using a pressure support ventilation technique. Dogs were studied when both central and peripheral chemoreceptors sensed transient hypocapnia induced by the pressure support ventilation and again with carotid body isolation such that only the central chemoreceptors sensed the hypocapnia. We observed that the CO₂ reserve was 4.5 Torr when the carotid chemoreceptors sensed the transient hypocapnia but more than doubled (>9 Torr) when only the central chemoreceptors sensed hypocapnia. Furthermore, the expiratory time prolongations observed when only central chemoreceptors were exposed to hypocapnia differed from those obtained when both the central and peripheral chemoreceptors sensed the hypocapnia in that they 1) were substantially shorter for a given reduction in end-tidal PCO₂, 2) showed no stimulus: response relationship with increasing hypocapnia, and 3) often occurred at a time (>45 s) beyond the latency expected for the central chemoreceptors. These findings agree with those previously obtained using an identical pressure support ventilation protocol in carotid body-denervated sleeping dogs (Nakayama H, Smith CA, Rodman JR, Skatrud JB, Dempsey JA. J Appl Physiol 94: 155–164, 2003). We conclude that hypocapnia sensed at the carotid body chemoreceptor is required for the initiation of apnea following a transient ventilatory overshoot in non-rapid eye movement sleep.

hypocapnia; carbon dioxide reserve; carbon dioxide sensitivity; sleep-disordered breathing; non-rapid eye movement sleep

This article has been cited by other articles:

				P. G. Guyenet The 2008 Carl Ludwig Lecture: retrotrapezoid nucleus, CO2 homeostasis, and breathing automaticity J Appl Physiol, August 1, 2008; 105(2): 404 - 416. [Abstract] [Full Text] [PDF]

				C. Julien, A. Bairam, and V. Joseph Chronic intermittent hypoxia reduces ventilatory long-term facilitation and enhances apnea frequency in newborn rats Am J Physiol Regulatory Integrative Comp Physiol, April 1, 2008; 294(4): R1356 - R1366. [Abstract] [Full Text] [PDF]