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Children's Hospital, Harvard Medical School, Boston 02115; and Veterans Affairs Medical Center, West Roxbury, Massachusetts 02132
Received 19 July 1995; accepted in final form 19 November 1996.
Zinkovska, Sophia, and Debra A. Kirby.
Intracerebroventricular propranolol prevented vascular resistance
increases on arousal from sleep apnea. J. Appl.
Physiol. 82(5): 1637-1643, 1997.
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 ± 3 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 µg/kg; a
-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
-adrenergic receptors in the central nervous system.
brain;
-adrenoreceptor; pig
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