Neural and local effects of hypoxia on cardiovascular responses to obstructive apnea

H. Schneider, C. D. Schaub, C. A. Chen, K. A. Andreoni, A. R. Schwartz, P. L. Smith, J. L. Robotham, C. P. O'Donnell

Research output: Contribution to journalArticlepeer-review

52 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)1093-1102
Number of pages10
JournalJournal of applied physiology
Issue number3
StatePublished - Mar 2000
Externally publishedYes


  • Autonomic nervous system
  • Canine
  • Hyperoxia
  • Pulmonary arterial pressure
  • Sleep
  • Systemic arterial pressure
  • Ventricular stroke volume

ASJC Scopus subject areas

  • General Medicine


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