Central sympathetic nervous system reinforcement in obstructive sleep apnoea

Wszędybył-Winklewska, Magdalena; Wolf, Jacek; Szarmach, Arkadiusz; Winklewski, Paweł J.; Szurowska, Edyta

doi:10.1016/j.smrv.2017.08.006

Cited by 11 publications

(6 citation statements)

References 161 publications

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“…BP and SAS fluctuations are further augmented by inspiratory resistance due to more negative intrathoracic pressures (reviewed by 1 ). In particular, more negative intrathoracic pressures lead to substantial increase in respiratory CSF shifts between cranial compartment and the cervical spinal canal (reviewed by 24 ). Thus, increased respiratory resistance should exacerbate the effects of slow breathing on the investigated variables.…”

Section: Introductionmentioning

confidence: 99%

Impact of slow breathing on the blood pressure and subarachnoid space width oscillations in humans

Nuckowska

Gruszecki

Kot

et al. 2019

Sci Rep

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The aim of the study was to assess cardiac and respiratory blood pressure (BP) and subarachnoid space (SAS) width oscillations during the resting state for slow and fast breathing and breathing against inspiratory resistance. Experiments were performed on a group of 20 healthy volunteers (8 males and 12 females; age 25.3 ± 7.9 years; BMI = 22.1 ± 3.2 kg/m 2 ). BP and heart rate (HR) were measured using continuous finger-pulse photoplethysmography. SAS signals were recorded using an SAS monitor. Oxyhaemoglobin saturation (SaO 2 ) and end-tidal CO 2 (EtCO 2 ) were measured using a medical monitoring system. Procedure 1 consisted of breathing spontaneously and at controlled rates of 6 breaths/minute and 6 breaths/minute with inspiratory resistance for 10 minutes. Procedure 2 consisted of breathing spontaneously and at controlled rates of 6, 12 and 18 breaths/minute for 5 minutes. Wavelet analysis with the Morlet mother wavelet was applied for delineation of BP and SAS signals cardiac and respiratory components. Slow breathing diminishes amplitude of cardiac BP and SAS oscillations. The overall increase in BP and SAS oscillations during slow breathing is driven by the respiratory component. Drop in cardiac component of BP amplitude evoked by slow-breathing may be perceived as a cardiovascular protective mechanism to avoid target organ damage. Further studies are warranted to assess long-term effects of slow breathing.

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Section: Introductionmentioning

confidence: 99%

Impact of slow breathing on the blood pressure and subarachnoid space width oscillations in humans

Nuckowska

Gruszecki

Kot

et al. 2019

Sci Rep

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“…Importantly, nITP less than or equal to Ϫ20 cmH 2 O has been documented in commonly encountered obstructive sleep apnea in adults, which should prompt research to clarify the physiological and pathophysiological mechanisms linking the two phenomena. This is of particular importance with respect to cerebrovascular diseases, as their clinical course may be influenced not only by BP load but also BP variability and CSF pulsatility (83).…”

Section: Discussionmentioning

confidence: 99%

“…Subsequently, the theory explaining bidirectional link between ICP and BP fluctuations with central role of sympathetic nervous system has gained physiologists' attraction (17,44,55,62,83). The hypothesis is that ICP fluctuations are linked to sympathetic activity in an opposite way as arterial baroreflex.…”

Section: Bp and Icp Oscillationsmentioning

confidence: 99%

Current understanding of the effects of inspiratory resistance on the interactions between systemic blood pressure, cerebral perfusion, intracranial pressure, and cerebrospinal fluid dynamics

Winklewski

Wolf

Gruszecki

et al. 2019

Journal of Applied Physiology

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Negative intrathoracic pressure (nITP) is generated by the respiratory muscles during inspiration to overcome inspiratory resistance, thus enabling lung ventilation. Recently developed noninvasive techniques have made it possible to assess the effects of nITP in real time in several physiological aspects such as systemic blood pressure (BP), intracranial pressure (ICP), and cerebral blood flow (CBF). It has been shown that nITP from 0 to −20 cmH2O elevates BP and diminishes ICP, which facilitates brain perfusion. The effects of nITP from −20 to −40 cmH2O on BP, ICP, and CBF remain largely unrecognized, yet even nITP at −40 cmH2O may facilitate CBF by diminishing ICP. Importantly, nITP from −20 to −40 cmH2O has been documented in adults in commonly encountered obstructive sleep apnea, which justifies research in this area. Recent revelations about interactions between ICP and BP have opened up new fields of research in physiological regulation and the pathophysiology of common diseases, such as hypertension, brain injury, and respiratory disorders. A better understanding of these interactions may translate directly into new therapies in various fields of clinical medicine.

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“…Intermittent hypoxia is associated with transient interruption to breathing resulting in transient cycles of oxygen desaturation and re-oxygenation, and can result from obstruction of airway passages and altered respiratory rhythm. Continued intermittent hypoxia chronically over time has deleterious effects as shown by the population cohort that suffers from obstructive sleep apnea (Neubauer, 2001;Wszedybyl-Winklewska et al, 2018). This cohort has been estimated to be 13% of the adult population (Peppard et al, 2013) and the resultant co-morbidities, including cardiovascular dysregulation and hypertension, contribute to poor prognosis and increased mortality (Lavie and Lavie, 2008).…”

Section: Chronic Intermittent Hypoxiamentioning

confidence: 99%

The Carotid Body a Common Denominator for Cardiovascular and Metabolic Dysfunction?

Badoer

2020

Front. Physiol.

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The carotid body is a highly vascularized organ designed to monitor oxygen levels. Reducing oxygen levels in blood results in increased activity of the carotid body cells and reflex increases in sympathetic nerve activity. A key contributor to elevated sympathetic nerve activity in neurogenic forms of hypertension is enhanced peripheral chemoreceptor activity. Hypertension commonly occurs in metabolic disorders, like obesity. Such metabolic diseases are serious global health problems. Yet, the mechanisms contributing to increased sympathetic nerve activity and hypertension in obesity are not fully understood and a better understanding is urgently required. In this review, we examine the literature that suggests that overactivity of the carotid body may also contribute to metabolic disturbances. The purine ATP is an important chemical mediator influencing the activity of the carotid body and the role of purines in the overactivity of the carotid body is explored. We will conclude with the suggestion that tonic overactivity of the carotid body may be a common denominator that contributes to the hypertension and metabolic dysfunction seen in conditions in which metabolic disease exists such as obesity or insulin resistance induced by high caloric intake. Therapeutic treatment targeting the carotid bodies may be a viable treatment since translation to the clinic could be more easily performed than expected via repurposing antagonists of purinergic receptors currently in clinical practice, and the use of other minimally invasive techniques that reduce the overactivity of the carotid bodies which may be developed for such clinical use.

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Central sympathetic nervous system reinforcement in obstructive sleep apnoea

Cited by 11 publications

References 161 publications

Impact of slow breathing on the blood pressure and subarachnoid space width oscillations in humans

Impact of slow breathing on the blood pressure and subarachnoid space width oscillations in humans

Current understanding of the effects of inspiratory resistance on the interactions between systemic blood pressure, cerebral perfusion, intracranial pressure, and cerebrospinal fluid dynamics

The Carotid Body a Common Denominator for Cardiovascular and Metabolic Dysfunction?

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