Effects of Exposure to Intermittent Hypoxia on Oxidative Stress and Acute Hypoxic Ventilatory Response in Humans

Pialoux, Vincent; Hanly, Patrick J.; Foster, Glen E.; Brugniaux, Julien V.; Beaudin, Andrew E.; Hartmann, Sara E.; Pun, Matiram; Duggan, Cailean T. C.; Poulin, Marc J.

doi:10.1164/rccm.200905-0671oc

Cited by 155 publications

(131 citation statements)

References 49 publications

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“…Interestingly, after 7 and 14 days of CIH, our model induced an increase in both acute isocapnic hypoxic ventilatory response and acute hyperoxic hypercapnic ventilatory response [25]. This was also reported for isocapnic hypoxic ventilatory response after 4 days of waking IH [26]. Moreover, using the same model, FOSTER et al [27] demonstrated changes in cardio-and cerebrovascular responses to acute hypoxia following exposure to intermittent hypoxia.…”

supporting

confidence: 81%

14 nights of intermittent hypoxia elevate daytime blood pressure and sympathetic activity in healthy humans

Tamisier¹,

Pépin²,

Rémy³

et al. 2010

European Respiratory Journal

252

168

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Obstructive sleep apnoea syndrome (OSAS) causes nocturnal chronic intermittent hypoxia (IH) that contributes to excess cardiovascular morbidity. To explore the consequences of IH, we used our recently developed model of nocturnal IH in healthy humans to characterise the profile of this blood pressure increase, to determine if it is sustained and to explore potential physiological mechanisms.We performed 24-h ambulatory monitoring of blood pressure in 12 healthy subjects before and after 2 weeks of IH exposure. We also assessed systemic haemodynamics, muscle sympathetic nerve activity (MSNA), ischaemic calf blood flow responses and baroreflex gain. We obtained blood samples for inflammatory markers before, during and after exposure. IH significantly increased daytime ambulatory blood pressure after a single night of exposure (3 mmHg for mean and diastolic) and further increased daytime pressures after 2 weeks of exposure (8 mmHg systolic and 5 mmHg diastolic). Mean¡SD MSNA increased across the exposure (17.2¡5.1 versus 21.7¡7.3 bursts?min -1 ; p,0.01) and baroreflex control of sympathetic outflow declined from -965.3¡375.1 to -598.4¡162.6 AIU?min -1 ?mmHg -1 (p,0.01). There were no evident changes in either vascular reactivity or systemic inflammatory markers. These data are the first to show that the arterial pressure rise is sustained throughout the waking hours beyond the acute phase immediately after exposure. Moreover, they may suggest that sympathoactivation induced by IH likely contributes to blood pressure elevation and may derive from reduced baroreflex inhibition. These mechanisms may reflect those underlying the blood pressure elevation associated with OSAS.

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supporting

confidence: 81%

14 nights of intermittent hypoxia elevate daytime blood pressure and sympathetic activity in healthy humans

Tamisier¹,

Pépin²,

Rémy³

et al. 2010

European Respiratory Journal

252

168

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“…64,65 The increase in inflammatory cytokines is thought to be related to repeated cycles of apneic oxygen desaturation and restoration. 44,[66][67][68][69][70] OSA has been shown to be an inflammatory process, associated with increased levels of systemic interleukin-2, interleukin-6, C-reactive protein, and tumor necrosis factor-alpha .…”

Section: Discussionmentioning

confidence: 99%

Obstructive Sleep Apnea and Incidence of Postoperative Delirium After Elective Knee Replacement in the Nondemented Elderly

Flink¹,

Rivelli²,

Cox³

et al. 2012

Survey of Anesthesiology

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“…[77][78][79][80][81][83][84][85][86] Long-term exposure to these recurrent episodes of hypoxiareoxygenation activate nicotinamide adenine dinucleotide phosphate-oxidase 2 that consumes oxygen through its generation of reactive oxygen species. [287][288][289][290][291] Tissue damage effected by these species is augmented by intermittent hypoxia reducing renal expression of antioxidants. 292 In addition, intermittent hypoxia induces the sympathetic nervous system to increase vascular resistance, downregulates expression of the kallikrein-kallistatin vasodilator Shelley Transforming growth factor β inhibition 446 Pro-fibrotic metalloproteinase inhibition 447 Anti-fibrotic metalloproteinase activation 447 Destabilization of renal Remote ischemic pre-conditioning [384][385][386][387][388][389][390] hypoxia-inducible factor Prolyl hydroxylase inhibition 244,448 von Hippel-Lindau protein inhibition 449 pathway, and activates the renal renin-angiotensin-aldosterone system to cause vasoconstriction.…”

Section: Repeated Episodes Of Acute Kidney Injurymentioning

confidence: 99%

Hypoxia: The Force that Drives Chronic Kidney Disease

Colgan

Shelley

2016

Clinical Medicine & Research

125

111

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In the United States the prevalence of end-stage renal disease (ESRD) reached epidemic proportions in 2012 with over 600,000 patients being treated. The rates of ESRD among the elderly are disproportionally high. Consequently, as life expectancy increases and the baby-boom generation reaches retirement age, the already heavy burden imposed by ESRD on the US health care system is set to increase dramatically. ESRD represents the terminal stage of chronic kidney disease (CKD). A large body of evidence indicating that CKD is driven by renal tissue hypoxia has led to the development of therapeutic strategies that increase kidney oxygenation and the contention that chronic hypoxia is the final common pathway to end-stage renal failure. Numerous studies have demonstrated that one of the most potent means by which hypoxic conditions within the kidney produce CKD is by inducing a sustained inflammatory attack by infiltrating leukocytes. Indispensable to this attack is the acquisition by leukocytes of an adhesive phenotype. It was thought that this process resulted exclusively from leukocytes responding to cytokines released from ischemic renal endothelium. However, recently it has been demonstrated that leukocytes also become activated independent of the hypoxic response of endothelial cells. It was found that this endothelium-independent mechanism involves leukocytes directly sensing hypoxia and responding by transcriptional induction of the genes that encode the β2-integrin family of adhesion molecules. This induction likely maintains the long-term inflammation by which hypoxia drives the pathogenesis of CKD. Consequently, targeting these transcriptional mechanisms would appear to represent a promising new therapeutic strategy.

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Effects of Exposure to Intermittent Hypoxia on Oxidative Stress and Acute Hypoxic Ventilatory Response in Humans

Cited by 155 publications

References 49 publications

14 nights of intermittent hypoxia elevate daytime blood pressure and sympathetic activity in healthy humans

14 nights of intermittent hypoxia elevate daytime blood pressure and sympathetic activity in healthy humans

Obstructive Sleep Apnea and Incidence of Postoperative Delirium After Elective Knee Replacement in the Nondemented Elderly

Hypoxia: The Force that Drives Chronic Kidney Disease

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