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This Article Full Text Free Full Text (PDF) Free All Versions of this Article: 98/4/1349    most recent 00706.2004v1 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 Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Web of Science (1) Citing Articles via Google Scholar Google Scholar Articles by O'Driscoll, D. M. Articles by Morrell, M. J. Search for Related Content PubMed PubMed Citation Articles by O'Driscoll, D. M. Articles by Morrell, M. J.

Occlusion of the upper airway does not augment the cardiovascular response to arousal from sleep in humans

¹Clinical and Academic Unit of Sleep and Breathing, National Heart and Lung Institute, Imperial College, and ²Sleep and Ventilation Unit, Royal Brompton Hospital, London, United Kingdom

Submitted 8 July 2004 ; accepted in final form 30 November 2004

The cardiovascular response to an arousal from sleep at the termination of an obstructive apnea is more than double that to a spontaneous arousal. We investigated the hypothesis that stimulation of respiratory mechanoreceptors, by inspiring against an occluded airway during an arousal from sleep, augments the accompanying cardiovascular response. Arousals (>10 s) from stage 2 sleep were induced by a 1-s auditory tone (85 dB) during a concomitant 1-s inspiratory occlusion (O) and without an occlusion [i.e., control arousal (C)] in 15 healthy men (mean ± SE: age, 25 ± 1 yr). Arousals were associated with a significant increase in mean arterial blood pressure (MAP) at 4 s (P < 0.001) and a significant decrease in R-R interval at 3 s (P < 0.001). However, the magnitude of the cardiovascular response was not different during C compared with O (MAP: C, 86 ± 3 to 104 ± 3 mmHg; O, 86 ± 3 to 105 ± 3 mmHg; P = 0.99. R-R interval: C, 1.12 ± 0.03 to 0.89 ± 0.04 s; O, 1.11 ± 0.02 to 0.87 ± 0.02 s, P = 0.99). Ventilation significantly increased during arousals under both conditions at the second breath (P < 0.001); this increase was not different between the two conditions (C: 4.40 ± 0.29 to 6.76 ± 0.61 l/min, O: 4.35 ± 0.34 to 7.65 ± 0.73 l/min; P = 0.31). We conclude that stimulation of the respiratory mechanoreceptors by transient upper airway occlusion is unlikely to interact with the arousal-related autonomic outflow to augment the cardiovascular response in healthy young men.

blood pressure; heart rate