Proceedings of The Physiological Society

University College Cork (2004) J Physiol 560P, C19

Communications

OCCLUSION OF THE UPPER AIRWAY DOES NOT AUGMENT THE CARDIOVASCULAR RESPONSE TO AROUSAL FROM SLEEP IN HUMANS.

O'Driscoll,Denise M; Kostikas,Konstantinos ; Simonds,Anita K; Morrell,Mary J;

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


Arousal from sleep at the termination of an obstructive apnoea is accompanied by a cardiovascular response which is more than double that to a spontaneous arousal (Okabe et al., 1995). Arousal at the termination of an obstructive apnoea occurs under conditions of hypercapnic hypoxia, occlusion of the upper airway and increasing negative intrathoracic pressure. We have previously reported that combined central and peripheral chemoreceptor stimulation using, hypercapnic hypoxia, does not interact with the arousal-related sympathetic outflow to augment the cardiovascular response in healthy humans (O′Driscoll et al., 2004). In the present study, we tested the hypothesis that stimulation of respiratory mechanoreceptors, by inspiring against an occluded airway, during an arousal from sleep augments the accompanying cardiovascular response. 15 healthy males (mean ± SEM: Age, 25 ± 1 yrs) were studied. Arousals (〉 10 s) were induced from Stage 2 NREM sleep 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)). The protocol was approved by the local ethics committee and all subjects gave written informed consent. The effects of time, and C versus O on cardiovascular and ventilatory responses to arousal were tested using ANOVA with repeated measures. Null hypotheses were rejected when p 〈 0.05. Arousals were associated with a significant increase in mean arterial blood pressure (MAP) at 4 s (p 〈 0.001) and a significant decrease in RR interval at 3 s (p 〈 0.001). However, the magnitude of the cardiovascular response was not different between C compared to O (MAP: C, 86 ± 3 to 104 ± 3 mmHg; O, 86 ± 3 to 105 ± 3 mmHg; p = 0.57. RR 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 2nd breath (p 〈 0.001); this increase was not different between the two conditions (C: 4.40 ± 0.29 to 6.76 ± 0.61 Lmin-1, O: 4.35 ± 0.34 to 7.65 ± 0.73 Lmin-1, p = 0.16). We conclude that stimulation of the respiratory mechanoreceptors by transient upper airway occlusion does not interact with the arousal-related autonomic outflow to augment the cardiovascular response in healthy young males.

Where applicable, experiments conform with Society ethical requirements