Effect of Autonomic Blockade on Heart Rate and Blood Pressure in Sleep Apnea Syndrome

To determine the impact of the autonomic nervous system on hemodynamic responses to sleep apnea we studied 7 male patients (486 years, BMI = 29.7 2.9 kg/m2) with an apnea index = 33 + 11/h. In two hypertensives, therapy was withdrawn 2 weeks before the study. During a full night polysomnography EEG, EOG, EMG, respiration, oximetry, heart rate (HR) and blood pressure (BP) (Finapres 23OOE) were recorded. Placebo and 3 short-acting autonomic blockers were randomly i.v. administered: antimuscarinic (atropine 1 mg, A), bT1 blocker (esmolol 40 mg, E), aL blocker (nicergoline 2.5 mg, N). A total of 367 obstructive apneas in NREM sleep were studied. With atropine, HR was increased at the beginning of apnea (P1) (74.5 2 bpm vs 65.4 2 bpm with placebo) and at the end apnea (P3) (76.6 1.9 bpm vs 67.1 1.76 bpm). At the resumption of breathing (RB), HR still increased (83.5 1.5bpm vs 80.1 bpm). Nicergoline had no significant effect on HR but significantly decreased SBP (117.8 1.4 mmHg vs 127 1.6 with placebo, p < 0,001). Nevertheless, the rise in BP from P3 to RB remained significant (p < 0.001). Esmolol significantly decreased HR at P1 (68.1 1.9 bpm vs 73.9 1.9 bpm) and at RB (75.9 1.9 vs 81.6 1.8).With A, the rise in HR at end-apnea (P3) suggests a vagal hyperactivity during this phase which is blunted at resumption when HR is unchanged. With N, HR remained equal to placebo values, but SBP and DBP decreased probably due to the activation of vascular sympathetic activity which lasts until resumption. With E, cardiac sympathetic activation was blunted during resumption. We conclude that apnea is characterized by a predominant vagal activity which abruptly disappears at resumption and a progressive rise in vascular and cardiac sympathetic activity which extends into resumption of breathing.