AN INDUCED BLOOD-PRESSURE RISE DOES NOT ALTER UPPER AIRWAY-RESISTANCEIN SLEEPING HUMANS

Sleep apnea is associated with episodic increases in systemic blood pr essure. We investigated whether transient increases in arterial pressu re altered upper airway resistance and/or breathing pattern in nine sl eeping humans (snorers and nonsnorers). A pressure-tipped catheter was placed below the base of the tongue, and flow was measured from a nos e or face mask. During non-rapid-eye-movement sleep, we injected 40- t o 200-mu g iv boluses of phenylephrine. Parasympathetic blockade was u sed if bradycardia was excessive. Mean arterial pressure (MAP) rose by 20 +/- 5 (mean +/-: SD) mmHg (range 12-37 mmHg) within 12 s and remai ned elevated for 105 s. There were no significant changes in inspirato ry or expiratory pharyngeal resistance (measured at peak flow, peak pr essure, 0.2 l/s or by evaluating the dynamic pressure-flow relationshi p). At peak MAP, end-tidal CO2 pressure fell by 1.5 Torr and remained low for 20-25 s. At 26 s after peak MAP, tidal volume fell by 19%, con sistent with hypocapnic ventilatory inhibition. We conclude that trans ient increases in MAP of a magnitude commonly observed during non-rapi d-eye-movement sleep-disordered breathing do not increase upper airway resistance and, therefore, will not perpetuate subsequent obstructive events.