Surges of muscle sympathetic nerve activity during obstructive apnea are linked to hypoxemia

Abstract

Obstructive sleep apnea (OSA) is associated with oscillations of arterial blood pressure (BP) that occur in phase with irregularities of respiration. To explore the role of the sympathetic nervous system in these responses, we studied muscle sympathetic nerve activity (MSNA; peroneal microneurography), an index of vasoconstrictor nerve traffic, and BP during awake regular breathing and during spontaneous apneas in patients with OSA. To determine the role of the arterial chemoreflex, we also examined the effects of 100% O2 (hyperoxia) on MSNA and BP. In awake regularly breathing patients with OSA (n = 12), resting MSNA was markedly higher than in an age-matched control population (n = 15) [41 +/- 23 (SD) vs. 24 +/- 17 bursts/min; P < 0.05] and was unchanged during hyperoxia (n = 9). Apneas during sleep (n = 8) were associated with surges in MSNA followed by transient rises in BP when breathing resumed. In contrast to room air apneas, hyperoxic apneas of similar duration were associated with attenuated MSNA responses (+82 +/- 84% vs. +5 +/- 25% compared with awake baseline; P < 0.05; n = 6), even though O2 did not affect sleep stage and the occurrence of arousal. Thus the BP oscillations that occur with apnea during sleep may in part be mediated by intermittent surges of sympathetic activity resulting in vasoconstriction. Because the MSNA responses to obstructive apnea are blunted during O2 administration, they appear to be linked to intermittent arterial hypoxemia and stimulation of arterial chemoreceptors.

Spontanous periodic breathing is associated with sympathetic hyperreactivity and baroreceptor dysfunction in hypertension

“…[5] It is likely that the same mechanisms are valid in humans too, since obstructive sleep apnea leads to increased SNS activity and increased daytime blood pressure. [6][7][8] Obstructive breathing disorders are associated with cardiovascular diseases such as hypertension, [9][10][11] myocardial infarction, [12] stroke, [13] and heart failure. [14] When treated with continuous positive airway pressure (CPAP) during sleep, daytime blood pressure and sympathetic activity decrease.…”

Effects of vagotomy on cardiovascular response to periodic apneas in sedated pigs

“…Reflex effects leading to changes in autonomic tone may be activated through 1) changes in thoracic mechanics from obstructed respiratory efforts (4), 2) changes in blood-gas tensions (hypoxia and/or hypercapnia) (12,18), and 3) postapneic arousals. These factors ultimately culminate in an increase in sympathoadrenal tone (9,13), which is associated with a pressor response during the apnea and postapnea periods. Studies to date have focused mainly on the relative effect of these physiological alterations with regard to the overall cardiovascular response to apneas.…”

“…Our data demonstrate that the pressor response to apneas in this model is dependent to a large extent on the vagus nerve. Sympathetic activation during periodic apneas is thought to occur from reflex effects elicited from hypoxia, possibly hypercapnia and mechanical alterations (6,9,12,13,18). These physiological alterations cause activation of peripheral and central sensors, including baroreceptors, chemoreceptors, and mechanoreceptors.…”

Relationship Between Sleep-Disordered Breathing Level and Acute Onset Time of Congestive Heart Failure

“…[10][11][12] SDB was related with heart strain due to apnea and various cardiovascular diseases. Some studies have reported a relationship between SDB and myocardial ischemia, 2,[13][14][15] arrhythmia, [16][17][18] sudden death, 19) platelet coagulation, 20) and inflammatory cytokines, 21,22) all of which may trigger heart failure.…”