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

Obstructive sleep apnea (OSA) acutely increases systemic (Psa) and pulmonar y (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 h ypoxia and the autonomic nervous system (ANS) in mediating these cardiovasc ular responses. Hyperoxia (40% oxygen) completely blocked any increase in P pa in response to obstructive apnea but only attenuated the increase in Psa . In contrast, after blockade of the ANS (20 mg/kg iv hexamethonium), obstr uctive 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 ris e 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 system ic 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 cou rse of the apnea.