Project Details


DESCRIPTION: (Adapted from the applicant's abstract and Specific Aims.)
Obstructive sleep apnea syndrome (OSAS) results in transient periods of
hypoxemia, hypercapnia and sleep interruption with associated acute and
chronic sympathoexcitation and hypertension. Treatment of the disorder
relieves many of the disorders and associated symptoms. The mechanism(s)
explaining the acute and chronic states of sympathoexcitation have not
been studied prospectively and may be relevant to the hypertension and
elevated cardiovascular mortality in OSAS. Abnormalities of chemoreflex
and baroreflex function have been speculated to explain the
cardiovascular consequences of OSAS, but have not been studied
prospectively.The Specific Aims are to: 1) determine the relative
contribution of hypoxemia, hypercapnia, and effects of inspiratory
effort to acute sympathoexcitation during sleep apnea or simulated apnea
during wakefulness in patients with OSAS and healthy subjects; 2)
develop a model of these reflex-mediated effects including interactive
effects between hypoxemia and hypercapnia in patients with OSAS and
healthy subjects; 3) determine the effect of sleep interruption on
baseline conditions, chemoreflex and baroreflex function in normotensive
and hypertensive patients with OSAS and in control subjects; 4)
determine the effect of short-term or long-term treatment of OSAS with
nasal CPAP on chronic sympathoexcitation, chemoreflex sensitivity and
baroreflex sensitivity during wakefulness; and 5) determine the relation
of chronic sympathoexcitation, chemoreflex sensitivity and baroreflex
sensitivity during wakefulness to the presence of clinical hypertension
in patients with OSAS. Understanding the control of sympathetic nerve
activity (SNA) in these patients may lead to improved management of this
condition and may lend provide new insight into the importance of
chemoreflex control of SNA in healthy and diseased humans.
Effective start/end date30/09/9431/08/00