INTRACEREBROVENTRICULAR PROPRANOLOL PREVENTED VASCULAR-RESISTANCE INCREASES ON AROUSAL FROM SLEEP-APNEA

Despite the increased risk of sudden cardiac death associated with sle ep apnea, little is known about mechanisms controlling cardiovascular responses to sleep apnea and arousal. Chronically instrumented pigs we re used to investigate the effects of airway obstruction (AO) during r apid-eye-movement (REM) and non-REM (NREM) sleep and arousal on mean a rterial pressure (MAP), heart rate (HR), cardiac output (GO), and tota l peripheral resistance (TPR). A stainless steel cannula was implanted in the lateral cerebral ventricle. During REM sleep, HR was 133 +/- 1 0 beats/min, MAP was 65 +/- 3 mmHg, CO was 1,435 +/- 69 ml/min, and TP R was 0.046 +/- 0.004 mmHg.ml(-1).min. During AO, CO decreased by 90 /- 17 ml/min (P < 0.05). On arousal from AO, MAP increased by 15 +/- 3 mmHg, HR increased by 10 +/- 3 beats/min, and TPR increased by 0.008 +/- 0.001 mmHg.ml(-1).min (all P < 0.05). Changes during NREM were sim ilar but were more modest during AO. After the intracerebroventricular administration of propranolol (50 mu g/kg; a beta-adrenoreceptor bloc king agent), decreases in CO during AO and increases in HR during arou sal were intact, but increases in MAP and TPR were no longer significa nt. These data suggest that vascular responses to AO during sleep may be regulated in part by beta-adrenergic receptors in the central nervo us system.