Muscle sympathetic nerve activity during central, mixed and obstructive apnea: Are there any differences?

Shimizu, Tetsuo; Takahashi, Yūji; Kogawa, Susumu; Takahashi, Ken­ichi; Saitō, Yasushi; Hishikawa, Yasuo; Broughton, Roger

doi:10.1111/j.1440-1819.1997.tb02607.x

Cited by 12 publications

(17 citation statements)

References 23 publications

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“…Another important pathological consequence of sleep apnea is increased sympathetic activity during sleep, which has important implications because increased sympathetic activity predicts poor survival in heart failure. Studies have reported that central apnea increases sympathetic activity as measured by microneurography, 56,57 overnight urinary excretion of norepinephrine, 58 and early morning plasma concentration of norepinephrine. 58 One study, 59 which measured sympathetic activity during daytime, also reported a higher activity in patients with central sleep apnea than those without.…”

Section: Pathophysiological Consequences Of Central Sleep Apneamentioning

confidence: 99%

Central Sleep Apnea in Congestive Heart Failure: Prevalence, Mechanisms, Impact, and Therapeutic Options

Javaheri

2005

Seminars in Respiratory and Critical Care Medicine

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Heart failure due to left ventricular systolic dysfunction is a prevalent syndrome and associated with morbidity, mortality, and huge economic cost. According to reports from several laboratories, a large number of patients with heart failure have central sleep apnea. Central sleep apnea causes arousals and sleep disruption, alters blood gases, and increases sympathetic activity. The pathophysiological consequences of central sleep apnea could adversely affect left ventricular structure and functions and worsen prognosis of heart failure. Several treatment options, including use of nocturnal supplemental oxygen, positive airway pressure devices, and theophylline have been systematically studied and have been shown to improve central sleep apnea. Long-term studies, however, are necessary to determine the impact of therapy on natural history of left ventricular systolic dysfunction.

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Section: Pathophysiological Consequences Of Central Sleep Apneamentioning

confidence: 99%

Central Sleep Apnea in Congestive Heart Failure: Prevalence, Mechanisms, Impact, and Therapeutic Options

Javaheri

2005

Seminars in Respiratory and Critical Care Medicine

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“…Obstructive and central apneas elicit entrained cyclical surges in efferent sympathetic vasoconstrictor discharge [1]–[3]. Relative to control participants, individuals with these two forms of sleep apnea exhibit increased central sympathetic outflow to skeletal muscle even during wakefulness [4], [5].…”

Section: Introductionmentioning

confidence: 99%

Apnea-Induced Cortical BOLD-fMRI and Peripheral Sympathoneural Firing Response Patterns of Awake Healthy Humans

2013

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End-expiratory breath-holds (BH) and Mueller manoeuvres (MM) elicit large increases in muscle sympathetic nerve activity (MSNA). In 16 healthy humans (9♀, 35±4 years) we used functional magnetic resonance imaging with blood oxygen level-dependent (BOLD) contrast to determine the cortical network associated with such sympathoexcitation. We hypothesized that increases in MSNA evoked by these simulated apneas are accompanied by BOLD contrast changes in the insular cortex, thalamus and limbic cortex. A series of 150 whole-brain images were collected during 3 randomly performed 16-second end-expiratory BHs and MMs (-30 mmHg). The identical protocol was repeated separately with MSNA recorded from the fibular nerve. The time course of the sympathoexcitatory response to both breathing tasks were correlated with whole-brain BOLD signal changes. Brain sites demonstrating both positive (activation) and negative (deactivation) correlations with the MSNA time course were identified. Sympathetic burst incidence increased (p<0.001) from 29±6 (rest) to 49±6 (BH) and 47±6 bursts/100 heartbeats (MM). Increased neural activity (Z-scores) was identified in the right posterior and anterior insular cortices (3.74, 3.64), dorsal anterior cingulate (3.42), fastigial and dentate cerebellar nuclei (3.02, 3.34). Signal intensity decreased in the left posterior insula (3.28) and ventral anterior cingulate (3.01). Apnea both activates and inhibits elements of a cortical network involved in the generation of sympathetic outflow. These findings identify a neuroanatomical substrate to guide future investigations into central mechanisms contributing to disorders characterized by elevated basal MSNA and exaggerated sympathetic responses to simulated apneas such as sleep apnea and heart failure.

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“…[1] It goes along with sympathetic activation; however the pattern of activation differs from obstructive apnea. [2] The resulting blood pressure elevation is blocked by the ganglionic blocker trimethaphan and thus neuronally mediated. Lowpressure receptors do not substantially contribute to sympathetic activation since endexpiratory breath holds and the sustained Mueller maneuver increase sympathetic activity to a similar extent despite different intra-thoracic pressure.…”

Section: Introductionmentioning

confidence: 99%

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

Binggeli

Sudano²,

Corti³

et al. 2010

Journal of Hypertension

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OBJECTIVES: Intermittent periods of hypoxemia such as during periodic breathing are associated with hypertension and increased sympathetic activity. In patients with sleep apnea syndrome, hypertension is common. Treating apnea improves hypertension and reduces sympathetic outflow. The aim of the present study was to investigate the phenomenon and mechanisms of spontaneous periodic breathing in patients with hypertension. METHOD: We examined 43 hypertensive patients with untreated hypertension without left-ventricular dysfunction, heart failure or sleep apnea syndrome. Muscle sympathetic nerve activity (MSA), heart rate (HR), blood pressure (BP) and respiration were continuously recorded at rest and during cold-pressor testing. Oxygen and a CO2-enriched gas were used to test central and peripheral chemoreceptors, respectively. Baroreceptor gain was measured using the alpha method. RESULTS: Seven out of 43 patients showed spontaneous periodic breathing while awake. No difference in MSA, HR and BP was seen between patients with and without periodic breathing at rest except the breathing pattern. However, the cold-pressor test caused a larger increase of MSA in patients with periodic breathing (203 +/-62 vs. 62 +/-8%, P < 0.0001 by ANOVA), as well as systolic (46 +/-6 vs. 25 +/-3 mmHg, P = 0.002) and diastolic BP (26 +/-5 vs. 12 +/-1 mmHg, P = 0.004, ANOVA). Baroreceptor gain was markedly higher in patients with periodic breathing. Chemoreceptor sensitivity was comparable. CONCLUSION: Spontaneous periodic breathing is relatively common in patients with hypertension and is associated with greatly enhanced responses to cold-pressor testing. We suggest increased baroreceptor gain and sympathetic outflow as a cause for the oscillatory respiration pattern via barorespiratory coupling.

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Muscle sympathetic nerve activity during central, mixed and obstructive apnea: Are there any differences?

Cited by 12 publications

References 23 publications

Central Sleep Apnea in Congestive Heart Failure: Prevalence, Mechanisms, Impact, and Therapeutic Options

Central Sleep Apnea in Congestive Heart Failure: Prevalence, Mechanisms, Impact, and Therapeutic Options

Apnea-Induced Cortical BOLD-fMRI and Peripheral Sympathoneural Firing Response Patterns of Awake Healthy Humans

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

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