Journal of Applied Physiology
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J Appl Physiol (May 10, 2007). doi:10.1152/japplphysiol.00017.2007
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Submitted on January 4, 2007
Accepted on May 8, 2007

THE APNEIC THRESHOLD DURING NON-REM SLEEP IN DOGS: SENSITIVITY OF CAROTID BODY VS. CENTRAL CHEMORECEPTORS

Curtis A. Smith1*, Bruno J. Chenuel2, Kathleen S. Henderson1, and Jerome A. Dempsey1

1 Department of Population Health Sciences, University of Wisconsin, Madison, Wisconsin, United States
2 Laboratoire de Physiologie, EA 3450., Faculté de Médecine de Nancy, Université Henri Poincaré, Vandoeuvre-lès-Nancy, France

* To whom correspondence should be addressed. E-mail: casmith4{at}wisc.edu.

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 (PETCO2 eupneic - PETCO2 apneic threshold) were determined using a pressure support ventilation (PSV) technique. Dogs were studied when both central and peripheral chemoreceptors sensed transient hypocapnia induced by the PSV and again with carotid body isolation such that only the central chemoreceptors sensed the hypocapnia. We observed that the CO2 reserve was {cong} 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 TE 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: a) were substantially shorter for a given reduction in PETCO2; b) showed no stimulus:response relationship with increasing hypocapnia; c) often occurred at a time (>45 seconds) beyond the latency expected for the central chemoreceptors. These findings agree with those previously obtained using an identical PSV protocol in carotid body denervated sleeping dogs. We conclude that hypocapnia sensed at the carotid body chemoreceptor is required for the initiation of apnea following a transient ventilatory overshoot in NREM sleep.




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