A physiological stimulus to upper airway receptors in humans

McBride, Brian F.; Whitelaw, W. A.

doi:10.1152/jappl.1981.51.5.1189

Cited by 111 publications

(35 citation statements)

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“…During an obstructive apnea, the nasal cavity is not exposed to pressure changes because the airway collapse occurs at the oropharynx (44). However, pressure-sensitive receptors have also been identified in the nasal cavity (30). In the present study, occlusion of the UA did not augment the cardiovascular response to an induced arousal, despite the likely addition of stimulation of receptors in the nose.…”

Section: Discussioncontrasting

confidence: 48%

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

O'Driscoll

Κostikas²,

Simonds³

et al. 2005

Journal of Applied Physiology

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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 (Ͼ10 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 Ϯ SE: age, 25 Ϯ 1 yr). Arousals were associated with a significant increase in mean arterial blood pressure (MAP) at 4 s (P Ͻ 0.001) and a significant decrease in R-R interval at 3 s (P Ͻ 0.001). However, the magnitude of the cardiovascular response was not different during C compared with O (MAP: C, 86 Ϯ 3 to 104 Ϯ 3 mmHg; O, 86 Ϯ 3 to 105 Ϯ 3 mmHg; P ϭ 0.99. R-R interval: C, 1.12 Ϯ 0.03 to 0.89 Ϯ 0.04 s; O, 1.11 Ϯ 0.02 to 0.87 Ϯ 0.02 s, P ϭ 0.99). Ventilation significantly increased during arousals under both conditions at the second breath (P Ͻ 0.001); this increase was not different between the two conditions (C: 4.40 Ϯ 0.29 to 6.76 Ϯ 0.61 l/min, O: 4.35 Ϯ 0.34 to 7.65 Ϯ 0.73 l/min; P ϭ 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 SPONTANEOUS AROUSAL FROM SLEEP is associated with large surges in both heart rate and blood pressure (13,42,49). In patients with obstructive sleep apnea (OSA), the surges in sympathetic activity that occur during an arousal from sleep at the termination of an apnea are more than double in size compared with a spontaneous arousal (2,29,40). Frequent cardiovascular surges in OSA have been implicated in the increased prevalence of both nocturnal and diurnal hypertension associated with OSA (37, 41). The mechanisms responsible for the augmentation of the cardiovascular response to arousal at the termination of an apnea potentially include stimulation of the chemoreceptors (hypercapnia, hypoxia), stimulation of upper airway (UA) mechanoreceptors (occlusion), stimulation of the pulmonary stretch receptors (increasing negative intrathoracic pressure, lung inflation), or arousalrelated central activation of autonomic centers. Our laboratory has previously reported in this journal that combined stimulation of the central and peripheral chemoreceptors (using hypercapnic hypoxia) does not significantly augment the cardiovascular response to arousal from sleep in healthy human subjects (39).Brief inspiratory occlusion evokes cortical activity during wakefulness (12, 15) and sleep (1, 51). Additionally, during sleep, complete airway occlusion can rapidly induce arousal, most likely as a result of afferent activity from UA mechanoreceptors to the brain stem respiratory centers (24). Altering this afferent activity, by topical anesthes...

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Section: Discussioncontrasting

confidence: 48%

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

O'Driscoll

Κostikas²,

Simonds³

et al. 2005

Journal of Applied Physiology

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“…The set-up allowing nasal breathing of subfreezing air without cooling the rest of the body was thought to be of importance, since there is evidence to suggest the existence of cold or airflow-sensitive receptors in the nasal cavity [5,6,16,17]. Consistent with these findings, there are reports indicating that cooling of the nasal cavity, and thus the inhalation of cold air through the nose, could induce bronchoconstriction [5,6,18].…”

Section: Discussionmentioning

confidence: 99%

Facial cooling, but not nasal breathing of cold air, induces bronchoconstriction: a study in asthmatic and healthy subjects

Koskela

Tukiainen²

1995

Eur Respir J

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Reflex-mediated bronchoconstriction in cold climates may be more important than it has previously been thought. This issue has seldom been studied using physiological methods. We wanted to investigate, using physiological methods, what triggers the bronchoconstriction occurring at cold ambient temperature during resting nasal ventilation: cooling of the skin of the face or cooling of the nasal cavity. Three experiments were carried out in 15 stable asthmatics and 10 healthy volunteers: 1) a whole-body exposure to subfreezing temperature in an environmental chamber, during which the subjects breathed cold air through the nose; 2) a similar exposure to subfreezing temperature except that the subjects now breathed warm air through the mouth from outside the chamber; and 3) nasal breathing of subfreezing air from a heat exchanger whilst the subjects sat at room temperature. Spirometric values and facial skin temperature were measured both during and after the exposures. Maximal decrements (means +/- standard errors) of forced expiratory volume in one second (FEV1) in experiments 1, 2 and 3 were: 5.8 +/- 0.8, 5.1 +/- 0.7 and 2.1 +/- 0.5%, respectively (p < 0.001). Only the two experiments in the environmental chamber induced significant bronchoconstriction. All responses were of similar magnitude in the asthmatic and the healthy subjects. The cooling of the skin of the face seems to be the trigger for the bronchoconstriction during resting nasal ventilation at cold ambient temperature both in asthmatic and nonasthmatic subjects.

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“…Inspiratory airflow cools the nose and larynx and stimulates cold receptors to cause a sensation of airway cooling which is associated with airflow. As well as providing a sensation of cool airflow, the stimulation of upper airway cold receptors causes a reflex inhibition of respiration and inhibition of upper airway accessory respiratory muscle activity in conscious man (McBride & Whitelaw 1981;Eccles & Tolley 1987) and in the anaesthetized dog (Mathew et al 1990). Inhalation of menthol causes the same reflex inhibition of respiration as a cold air stimulus but without any change in airway temperature in the anaesthetized guinea-pig (Orani et al 1991), the anaesthetized dog (Sant' Ambrogio et al 1992), and in conscious man (Eccles et al 1989;De Cort et al 1993;Sloan et al 1993).…”

Section: Respiratory Systemmentioning

confidence: 99%

Menthol and Related Cooling Compounds

Eccles

1994

Journal of Pharmacy and Pharmacology

420

334

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ToxicologySummary-Menthol and related cooling compounds such as 'coolant agent lo', are widely used in products ranging from common cold medications to toothpastes, confectionery, cosmetics and pesticides. The review brings together a range of information on production and chemistry of menthol, and its metabolism, mechanism of action, structure-activity relationships, pharmacology and toxicology. In particular, the coolant action and carminative actions of menthol are discussed in terms of actions on calcium conductance in sensory nerves and smooth muscle. The actions of menthol on the nose, respiratory reflexes, oral cavity, skin and gastrointestinal tract are reviewed.

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A physiological stimulus to upper airway receptors in humans

Cited by 111 publications

References 0 publications

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

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

Facial cooling, but not nasal breathing of cold air, induces bronchoconstriction: a study in asthmatic and healthy subjects

Menthol and Related Cooling Compounds

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