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

• Published in: Journal of applied physiology (1985) 2007-08, Vol.103 (2), p.578-586
• Main Authors: Smith, C. A, Chenuel, B. J, Henderson, K. S, Dempsey, J. A
• Format: Article
• Language: English
• Subjects: Animals; Apnea - etiology; Apnea - physiopathology; Biological and medical sciences; Brain - blood supply; Carbon dioxide; Carbon Dioxide - metabolism; Carotid Body - physiology; Chemoreceptor Cells - physiology; Disease Susceptibility - physiopathology; Dogs; Eye movements; Female; Fundamental and applied biological sciences. Psychology; Hypocapnia - physiopathology; Regional Blood Flow - physiology; Sleep apnea; Sleep, REM - physiology; Studies
• ISSN: 8750-7587; 1522-1601
• DOI: 10.1152/japplphysiol.00017.2007

1 John Rankin Laboratory of Pulmonary Medicine and Department of Population Health Sciences, University of Wisconsin, Madison, Wisconsin; and 2 Laboratoire 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 CO 2 reserve (end-tidal P CO 2 eupneic – end-tidal P CO 2 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 CO 2 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 P CO 2 , 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 Address for reprint requests and other correspondence: C. A. Smith, 4245 MSC, 1300 Univ. Ave., Madison, WI 53706 (e-mail: casmith4{at}wisc.edu )