Effects of arousal and sleep state on systemic and pulmonary hemodynamics in obstructive apnea

During obstructive sleep apnea (OSA), systemic (Psa) and pulmonary (Ppa) ar terial pressures acutely increase after apnea termination, whereas left and right ventricular stroke volumes (SV) reach a nadir. In a canine model (n = 6), we examined the effects of arousal, parasympathetic blockade (atropin e 1 mg/kg iv), and sleep state on cardiovascular responses to OSA. In the a bsence of arousal, SV remained constant after apnea termination, compared w ith a 4.4 +/- 1.7% decrease after apnea with arousal (P < 0.025). The rise in transmural Ppa was independent of arousal (4.5 +/- 1.0 vs. 4.1 +/- 1.2 m mHg with and without arousal, respectively), whereas Psa increased more aft er apnea termination in apneas with arousal compared with apneas without ar ousal. Parasympathetic blockade abolished the arousal-induced increase in P sa, indicating that arousal is associated with a vagal withdrawal of the pa rasympathetic tone to the heart. Rapid-eye-movement (REM) sleep blunted the increase in Psa (pre- to end-apnea: 5.6 +/- 2.3 mmHg vs. 10.3 +/- 1.6 mmHg , REM vs. non-REM, respectively, P < 0.025), but not transmural Ppa, during an obstructive apnea. We conclude that arousal and sleep state both have d ifferential effects on the systemic and pulmonary circulation in OSA, indic ating that, in patients with underlying cardiovascular disease, the hemodyn amic consequences of OSA may be different for the right or the left side of the circulation.