Neurocirculatory consequences of abrupt change in sleep state in
humans.
Morgan, Barbara J., David C. Crabtree, Dominic S. Puleo, M. Safwan
Badr, Fredy Toiber, and James B. Skatrud.
Departments of Kinesiology and Medicine, University of Wisconsin
and the Middleton Memorial Veterans Hospital, Madison, Wisconsin
53706
APStracts 3:0095A, 1996.
The arterial pressure elevations which accompany sleep apneas may be
caused by chemoreflex stimulation, negative intrathoracic pressure,
and/or arousal. To assess the neurocirculatory effects of arousal
alone, we applied graded auditory stimuli during NREM sleep in 8
healthy humans. We measured muscle sympathetic nerve activity
(intraneural microelectrodes), electroencephalogram (C4/A1, O1/A2),
arterial pressure (photoelectric plethysmography), heart rate (ECG),
and stroke volume (impedance cardiography). Auditory stimuli caused
abrupt increases in systolic and diastolic pressure (+21+/-2 and
+15+/-1 mmHg) and heart rate (+11+/-2 beats/min). Cardiac output
decreased (-10%). Stimuli that produced EEG evidence of arousal
evoked 1-2 large bursts of sympathetic activity (316+/-46% of
baseline amplitude). Stimuli that did not alter EEG frequency
produced smaller but consistent pressor responses even though no
sympathetic activation was observed. We conclude that arousal from
NREM sleep evokes a pressor response caused by increased peripheral
vascular resistance. Increased sympathetic outflow to skeletal muscle
may contribute to, but is not required for, this vasoconstriction.
The neurocirculatory effects of arousal may augment those caused by
asphyxia during episodes of sleep disordered breathing.
Received 19 June 1995; accepted in final form 2 January 1996.
APS Manuscript Number A650-5.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 14 February 96