Airway obstruction during sleep increases blood pressure without
arousal.
O'donnell, C. P., Ayuse, T., King, E. D., Schwartz, A. R, Smith, P.
L., Robotham, J. L.
Department of Anesthesiology and Critical Care Medicine, Pulmonary
Anesthesia Laboratory, and Department of Medicine, Division of
Pulmonary and Critical Care Medicine, Johns Hopkins University,
Baltimore, Maryland, USA
APStracts 2:0499A, 1995.
Recent studies suggest that arousal is the dominant factor acutely
increasing blood pressure in obstructive sleep apnea (OSA), 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 OSA was used to
examine the relative contributions of these mechanisms in the blood
pressure response to induced airway obstruction during NREM sleep. In
Part A of the study, the arousal response was eliminated from an
obstructive event by restoring airway patency just prior to 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 (ANS) with hexamethonium (20
mg/kg i.v.), 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) show that
obstructive apneic events of 28.5 + 3.1 secs 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 (P < 0.005) in the absence of arousal. 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), there was
no change in MAP during the obstructive apneic event, and MAP fell by
more than 10 mmHg (P < 0.05) in the post-obstruction period,
whether or not arousal occurred. 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.
Received 2 February 1995; accepted in final form 27 October 1995.
APS Manuscript Number A127-5.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 30 November 95