title: Airway obstruction during sleep increases blood pressure without arousal.
abstract: Recent studies suggest that arousal is the dominant factor acutely increasing blood pressure in obstructive sleep apnea and that neither stimulation of chemoreceptors nor mechanical factors associated with large negative swings in intrapleural pressure substantially contribute to the rise in blood pressure associated with each obstructive apneic event. A canine model of obstructive sleep apnea was used to examine the relative contributions of these mechanisms in the blood pressure response to induced airway obstruction during non-rapid-eye-movement sleep. In part A of the study, the arousal response was eliminated from an obstructive event by restoring airway patency just before the expected arousal, allowing blood pressure responses to be compared between obstructive events with and without arousal. In part B of the study, the protocol of Part A was repeated after pharmacological blockade of the autonomic nervous system with hexamethonium (20 mg/kg iv), eliminating neurally mediated responses due to arousal, stimulation of chemoreceptors, or other reflexes, while maintaining any mechanical effects on blood pressure related to swings in intrapleural pressure. The results of part A (n = 4 dogs) show that obstructive apneic events of 28.5 +/- 3.1 s duration, with arterial hemoglobin desaturation to 92.9 +/- 0.8% and airway pressure swings of -37.6 +/- 6 mmHg, significantly increased mean arterial pressure (MAP) by 13.8 +/- 1.5 mmHg in the absence of arousal (P < 0.005). In comparison, when arousal was allowed to occur, MAP increased by a further 11.8 +/- 1.2 mmHg (P < 0.01). In part B (n = 3 dogs), there was no change in MAP during the obstructive apneic event, and MAP fell by > 10 mmHg in the postobstruction period whether or not arousal occurred (P < 0.05). We conclude that neural reflexes, but not mechanical factors, substantially contribute to the acute blood pressure response to an obstructive apneic event and that arousal produces a separate, additional acute hypertensive response.
authors.affiliation: Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University, Baltimore, Maryland 21224, USA.
authors.forename: C P
authors.initials: CP
authors.lastname: O'Donnell
authors.forename: T
authors.initials: T
authors.lastname: Ayuse
authors.forename: E D
authors.initials: ED
authors.lastname: King
authors.forename: A R
authors.initials: AR
authors.lastname: Schwartz
authors.forename: P L
authors.initials: PL
authors.lastname: Smith
authors.forename: J L
authors.initials: JL
authors.lastname: Robotham
mesh_terms: D000818:Animals; D001049:Apnea / Q000503:physiopathology*; D001143:Arousal / Q000502:physiology*; D001794:Blood Pressure / Q000502:physiology*; D004285:Dogs; D004569:Electroencephalography; D005260:Female; D006339:Heart Rate / Q000502:physiology*; D008297:Male; D012890:Sleep / Q000502:physiology*; D012892:Sleep Deprivation