Intracerebroventricular propranolol prevented vascular resistance increases on arousal from sleep apnea

Despite the increased risk of sudden cardiac death associated with sleep apnea, little is known about mechanisms controlling cardiovascular responses to sleep apnea and arousal. Chronically instrumented pigs were used to investigate the effects of airway obstruction (AO) during rapid-eye-movement (REM) and non-REM (NREM) sleep and arousal on mean arterial pressure (MAP), heart rate (HR), cardiac output (CO), and total peripheral resistance (TPR). A stainless steel cannula was implanted in the lateral cerebral ventricle. During REM sleep, HR was 133 +/- 10 beats/min, MAP was 65 +/- 8 mmHg, CO was 1,435 +/- 69 ml/min, and TPR 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 similar but were more modest during AO. After the intracerebroventricular administration of propranolol (50 micrograms/kg; a beta-adrenoreceptor blocking agent), decreases in CO during AO and increases in HR during arousal were intact, but increases in MAP and TPR were no longer significant. These data suggest that vascular responses to AO during sleep may be regulated in part by beta-adrenergic receptors in the central nervous system.