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Department of Medicine, Division of Pulmonary and Critical Care Medicine, Department of Anesthesiology and Critical Care Medicine, and Department of Surgery, Johns Hopkins University, Baltimore, Maryland 21224
Obstructive sleep apnea (OSA) acutely
increases systemic (Psa) and pulmonary (Ppa) arterial pressures and
decreases ventricular stroke volume (SV). In this study,
we used a canine model of OSA (n = 6) to examine the role of
hypoxia and the autonomic nervous system (ANS) in mediating these
cardiovascular responses. Hyperoxia (40% oxygen) completely blocked
any increase in Ppa in response to obstructive apnea but only
attenuated the increase in Psa. In contrast, after blockade of the ANS
(20 mg/kg iv hexamethonium), obstructive apnea produced a decrease in
Psa (
5.9 mmHg; P < 0.05) but no change in Ppa, and the
fall in SV was abolished. Both the fall in Psa and the rise in Ppa that
persisted after ANS blockade were abolished when apneas were induced
during hyperoxia. We conclude that 1) hypoxia can account for
all of the Ppa and the majority of the Psa response to obstructive
apnea, 2) the ANS increases Psa but not Ppa in obstructive
apnea, 3) the local effects of hypoxia associated with
obstructive apnea cause vasodilation in the systemic vasculature and
vasoconstriction in the pulmonary vasculature, and 4) a rise in
Psa acts as an afterload to the heart and decreases SV over the
course of the apnea.
autonomic nervous system; canine; hyperoxia; pulmonary arterial pressure; sleep; systemic arterial pressure; ventricular stroke volume
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