AIRWAY-OBSTRUCTION DURING SLEEP INCREASES BLOOD-PRESSURE WITHOUT AROUSAL

Recent studies suggest that arousal is the dominant factor acutely inc reasing blood pressure in obstructive sleep apnea and that neither sti mulation of chemoreceptors nor mechanical factors associated with larg e negative swings in intrapleural pressure substantially contribute to the rise in blood pressure associated with each obstructive apneic ev ent. A canine model of obstructive sleep apnea was used to examine the relative contributions of these mechanisms in the blood pressure resp onse 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 obs tructive 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 chemorecep tors, or other reflexes, while maintaining any mechanical effects on b lood 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 incre ased 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 occ ur, 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 apnei c event, and MAP fell by >10 mmHg in the postobstruction period whethe r or not arousal occurred (P < 0.05). We conclude that neural reflexes , but not mechanical factors, substantially contribute to the acute bl ood pressure response to an obstructive apneic event and that arousal produces a separate, additional acute hypertensive response.