NEUROCIRCULATORY CONSEQUENCES OF ABRUPT CHANGE IN SLEEP STATE IN HUMANS

The arterial pressure elevations that accompany sleep apneas may be ca used by chemoreflex stimulation, negative intrathoracic pressure, and/ or arousal. To assess the neurocirculatory effects of arousal alone, w e applied graded auditory stimuli during non-rapid-eye-movement (NREM) sleep in eight healthy humans. We measured muscle sympathetic nerve a ctivity (intraneural microelectrodes), electroencephalogram (EEG; C-4/ A(1) and O-1/A(2)), arterial pressure (photoelectric plethysmography), heart rate (electrocardiogram), and stroke volume (impedance cardiogr aphy). Auditory stimuli caused abrupt increases in systolic and diasto lic pressures (21 +/- 2 and 15 +/- 1 mmHg) and heart rate (11 +/- 2 be ats/min). Cardiac output decreased (-10%). Stimuli that produced EEG e vidence of arousal evoked one to two large bursts of sympathetic activ ity (316 +/- 46% of baseline amplitude). Stimuli that did not alter EE G frequency produced smaller but consistent presser responses even tho ugh no sympathetic activation was observed. We conclude that arousal f rom NREM sleep evokes a presser response caused by increased periphera l vascular resistance. Increased sympathetic outflow to skeletal muscl e may contribute to, but is not required for, this vasoconstriction. T he neurocirculatory effects of arousal may augment those caused by asp hyxia during episodes of sleep-disordered breathing.