Normal hypercapnic cerebrovascular conductance in obstructive sleep apnea

Ryan, Clodagh M.; Battisti‐Charbonney, Anne; Sobczyk, Olivia; Duffin, James; Fisher, Joseph A.

doi:10.1016/j.resp.2013.09.003

Cited by 10 publications

(12 citation statements)

References 32 publications

(48 reference statements)

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“…Finally, studies assessing CBF responses to a standardized breath hold have all reported OSA patients to have a lower CBF response compared to control subjects (Siebler & Nachtmann, 1993;Diomedi et al 1998;Placidi et al 1998;Prilipko et al 2014;Coloma Navarro et al 2016). Thus, it is of note that Ryan et al (2014) found no difference between OSA patients and control subjects in response to a hypoxic-hypercapnic challenge. Thus, it is of note that Ryan et al (2014) found no difference between OSA patients and control subjects in response to a hypoxic-hypercapnic challenge.…”

Section: Sympathetic Functionmentioning

confidence: 66%

“…Although the principal stimulus to CBF during breath holds is A. E. Beaudin and others hypercapnia (Przybylowski et al 2003), breath holds have a degree of hypoxia, particularly if prolonged. Thus, it is of note that Ryan et al (2014) found no difference between OSA patients and control subjects in response to a hypoxic-hypercapnic challenge. Therefore, current data indicate that OSA patients have an impaired cerebrovascular response to hypoxia that is associated with OSA severity, but there is still debate regarding the impact of OSA on the hypercapnic CBF response.…”

Section: Sympathetic Functionmentioning

confidence: 66%

“…Using a progressive hyperoxic hypercapnic challenge, one study reported that OSA patients had lower CBF responses compared with age-matched control subjects (Reichmuth et al 2009), while the same group also found that the CBF response to hypercapnia was negatively correlated with AHI and positively correlated with the mean S aO 2 during sleep . Subsequently, Ryan et al (2014) found no difference in the CBF response to progressive hyperoxic hypercapnia between OSA patients and age-and BMI-matched control subjects. Finally, studies assessing CBF responses to a standardized breath hold have all reported OSA patients to have a lower CBF response compared to control subjects (Siebler & Nachtmann, 1993;Diomedi et al 1998;Placidi et al 1998;Prilipko et al 2014;Coloma Navarro et al 2016).…”

Section: Sympathetic Functionmentioning

confidence: 93%

“…All studies using steady-state hypercapnic challenges report that OSA patients have similar responses to non-OSA control subjects (Urbano et al 2008;Foster et al 2009b). Subsequently, Ryan et al (2014) found no difference in the CBF response to progressive hyperoxic hypercapnia between OSA patients and age-and BMI-matched control subjects. Subsequently, Ryan et al (2014) found no difference in the CBF response to progressive hyperoxic hypercapnia between OSA patients and age-and BMI-matched control subjects.…”

Section: Sympathetic Functionmentioning

confidence: 99%

“…Contrary to hypoxia, there are fewer studies assessing the pressor response to hypercapnia, but the results are more consistent; OSA is not associated with an elevated pressor response to hypercapnia (Reichmuth et al 2009;Foster et al 2009b;Ryan et al 2014).…”

Section: Sympathetic Functionmentioning

confidence: 99%

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Impact of obstructive sleep apnoea and intermittent hypoxia on cardiovascular and cerebrovascular regulation

Beaudin

Waltz

Hanly

et al. 2017

Experimental Physiology

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What is the topic of this review? This review examines the notion that obstructive sleep apnoea (OSA) and intermittent hypoxia (IH) have hormetic effects on vascular health. What advances does it highlight? Clinical (OSA patient) and experimental animal and human models report that IH is detrimental to vascular regulation. However, mild IH and, by extension, mild OSA also have physiological and clinical benefits. This review highlights clinical and experimental animal and human data linking OSA and IH to vascular disease and discusses how hormetic effects of OSA and IH relate to OSA severity, IH intensity and duration, and patient/subject age. Obstructive sleep apnoea (OSA) is associated with increased risk of cardiovascular and cerebrovascular disease, a consequence attributed in part to chronic intermittent hypoxia (IH) resulting from repetitive apnoeas during sleep. Although findings from experimental animal, and human, models have shown that IH is detrimental to vascular regulation, the severity of IH used in many of these animal studies [e.g. inspired fraction of oxygen (FI,O2) = 2-3%; oxygen desaturation index = 120 events h ] is considerably greater than that observed in the majority of patients with OSA. This may also explain disparities between animal and recently developed human models of IH, where IH severity is, by necessity, less severe (e.g. FI,O2 = 10-12%; oxygen desaturation index = 15-30 events h ). In this review, we highlight the current knowledge regarding the impact of OSA and IH on cardiovascular and cerebrovascular regulation. In addition, we critically discuss the recent notion that OSA and IH may have hormetic effects on vascular health depending on conditions such as OSA severity, IH intensity and duration, and age. In general, data support an independent causal link between OSA and vascular disease, particularly for patients with severe OSA. However, the data are equivocal for older OSA patients and patients with mild OSA, because advanced age and short-duration, low-intensity IH have been reported to provide a degree of protection against IH and ischaemic events such as myocardial infarction and stroke, respectively. Overall, additional studies are needed to investigate the beneficial/detrimental effects of mild OSA on the various vascular beds.

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Section: Sympathetic Functionmentioning

confidence: 66%

Section: Sympathetic Functionmentioning

confidence: 66%

Section: Sympathetic Functionmentioning

confidence: 93%

Section: Sympathetic Functionmentioning

confidence: 99%

Section: Sympathetic Functionmentioning

confidence: 99%

See 3 more Smart Citations

Impact of obstructive sleep apnoea and intermittent hypoxia on cardiovascular and cerebrovascular regulation

Beaudin

Waltz

Hanly

et al. 2017

Experimental Physiology

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Evaluation of Cerebrovascular Reactivity in Subjects with and without Obstructive Sleep Apnea

Ryan

Battisti‐Charbonney

Sobczyk

et al. 2018

Journal of Stroke and Cerebrovascular Diseases

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Vascular responses to hypoxia are not impaired in obstructive sleep apnoea patients free of overt cardiovascular disease

Beaudin

Hanly

Raneri

et al. 2019

Experimental Physiology

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New Findings What is the central question of this study?Does treatment of obstructive sleep apnoea (OSA) with nocturnal oxygen or continuous positive airway pressure (CPAP) improve hypoxic vascular responses, which are reportedly impaired in OSA? What is the main finding and its importance?Cerebrovascular and cardiovascular hypoxic responses were not impaired in OSA patients free of overt cardiovascular disease and known risk factors, and were not altered by nocturnal oxygen or CPAP treatment. We conclude that this OSA patient phenotype has normal vascular responses to hypoxia and is unlikely to obtain long term cardiovascular benefits from nocturnal oxygen or CPAP therapy. Abstract Cerebral blood flow (CBF) and cardiovascular responses to hypoxia are reportedly impaired in obstructive sleep apnoea (OSA) patients and corrected by continuous positive airway pressure (CPAP), beneficial effects that are ascribed to correction of OSA‐related intermittent hypoxia (IH). However, CPAP corrects both IH and ancillary OSA features (i.e. intermittent hypercapnia, sympathetic activation, blood pressure surges, negative intrathoracic pressure swings and sleep fragmentation). Whether correction of these ancillary OSA features contribute to CPAP's beneficial effects on vascular hypoxic responses is unknown. Nocturnal oxygen corrects OSA‐induced IH, but apnoeas and ancillary features persist. Thus, we examined the effects of nocturnal oxygen and CPAP on cerebrovascular and cardiovascular hypoxic responses in untreated OSA patients. Responses were assessed in 52 OSA patients free of overt cardiovascular disease and known risk factors at baseline, after 2 weeks of nocturnal oxygen (n = 26) or no treatment (n = 26), and after ∼4 weeks of CPAP treatment (n = 40). Twenty‐two age‐matched controls were assessed at baseline and follow‐up visits. Resting, isocapnic euoxia mean blood pressure was decreased following nocturnal oxygen (−3.6 ± 6.0 mmHg; P = 0.006) and CPAP (−4.5 ± 7.5 mmHg; P < 0.001) while cerebrovascular conductance was increased with CPAP (P = 0.001). However, these changes were not different from controls. Unexpectedly, OSA patients and controls had similar hypoxic vascular responses at baseline that were not changed by either nocturnal oxygen or CPAP. We conclude that OSA patients free of overt cardiovascular disease and known risk factors did not have impaired cerebrovascular or cardiovascular responses to hypoxia and are unlikely to obtain long term cardiovascular benefits from nocturnal oxygen or CPAP therapy.

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Normal hypercapnic cerebrovascular conductance in obstructive sleep apnea

Cited by 10 publications

References 32 publications

Impact of obstructive sleep apnoea and intermittent hypoxia on cardiovascular and cerebrovascular regulation

Impact of obstructive sleep apnoea and intermittent hypoxia on cardiovascular and cerebrovascular regulation

Evaluation of Cerebrovascular Reactivity in Subjects with and without Obstructive Sleep Apnea

Vascular responses to hypoxia are not impaired in obstructive sleep apnoea patients free of overt cardiovascular disease

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