Invited Review: Physiological and pathophysiological responses to intermittent hypoxia

Neubauer, Judith A.

doi:10.1152/jappl.2001.90.4.1593

Cited by 261 publications

(183 citation statements)

References 79 publications

(75 reference statements)

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“…27 Furthermore, the desaturation-reoxygenation sequence characterizing intermittent hypoxia constitutes a major stimulus, even more potent than continuous hypoxia, which leads to oxidative stress, systemic inflammation, and generalized vascular endothelial damage adversely affecting myocardial function. 25,28 The present study also shows that SBDs and especially OSA is common in IPF extending previous observations. 2,3 This rate of occurrence is even higher from the 10% of OSA encountered in chronic obstructive pulmonary disease (COPD), rendering the term "overlap" syndrome even more appropriate for the coexistence of OSA and IPF.…”

Section: Discussionsupporting

confidence: 90%

Sleep Oxygen Desaturation Predicts Survival in Idiopathic Pulmonary Fibrosis

Kolilekas

Manali

Vlami

et al. 2013

Journal of Clinical Sleep Medicine

119

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background: Recent studies suggest poor sleep quality in patients with idiopathic pulmonary fi brosis (IPF). However, so far, the impact of IPF-related sleep breathing disorders (SBDs) on survival has not been extensively studied. Methods: In a cohort of 31 (24 males) treatment-naïve, newly diagnosed consecutive IPF patients, we prospectively investigated the relationship of SBD parameters such as apnea-hypopnea index (AHI), maximal difference in oxygen saturation between wakefulness and sleep (maxdiff SpO 2 ), and lowest sleep oxygen saturation (lowest SpO 2 ) with clinical (survival, dyspnea, daytime sleepiness), pulmonary function, submaximal (6-min walk test [6MWT]) and maximal exercise variables (cardiopulmonary exercise test [CPET]), and right ventricular systolic pressure (RVSP). Results: Sleep oxygen desaturation exceeded signifi cantly that of maximal exercise (p < 0.001). Maxdiff SpO 2 was inversely related to survival, DLCO%, and SpO 2 after 6MWT, and directly with dyspnea, AHI, and RVSP. The lowest SpO 2 was directly related to survival and to functional (TLC%, DLCO%) as well as submaximal and maximal exercise variables (6MWT

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Section: Discussionsupporting

confidence: 90%

Sleep Oxygen Desaturation Predicts Survival in Idiopathic Pulmonary Fibrosis

Kolilekas

Manali

Vlami

et al. 2013

Journal of Clinical Sleep Medicine

119

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“…Several of these categories are the topics of other reviews in this series or were topics of previous reviews in the Journal of Applied Physiology (80,166,178,198).…”

Section: Models Of Respiratory Plasticitymentioning

confidence: 99%

Invited Review: Neuroplasticity in respiratory motor control

Mitchell

Johnson

2003

Journal of Applied Physiology

351

313

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Although recent evidence demonstrates considerable neuroplasticity in the respiratory control system, a comprehensive conceptual framework is lacking. Our goals in this review are to define plasticity (and related neural properties) as it pertains to respiratory control and to discuss potential sites, mechanisms, and known categories of respiratory plasticity. Respiratory plasticity is defined as a persistent change in the neural control system based on prior experience. Plasticity may involve structural and/or functional alterations (most commonly both) and can arise from multiple cellular/synaptic mechanisms at different sites in the respiratory control system. Respiratory neuroplasticity is critically dependent on the establishment of necessary preconditions, the stimulus paradigm, the balance between opposing modulatory systems, age, gender, and genetics. Respiratory plasticity can be induced by hypoxia, hypercapnia, exercise, injury, stress, and pharmacological interventions or conditioning and occurs during development as well as in adults. Developmental plasticity is induced by experiences (e.g., altered respiratory gases) during sensitive developmental periods, thereby altering mature respiratory control. The same experience later in life has little or no effect. In adults, neuromodulation plays a prominent role in several forms of respiratory plasticity. For example, serotonergic modulation is thought to initiate and/or maintain respiratory plasticity following intermittent hypoxia, repeated hypercapnic exercise, spinal sensory denervation, spinal cord injury, and at least some conditioned reflexes. Considerable work is necessary before we fully appreciate the biological significance of respiratory plasticity, its underlying cellular/molecular and network mechanisms, and the potential to harness respiratory plasticity as a therapeutic tool.

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“…Intermittent hypoxia (IH) is one of the major components of obstructive sleep apnea syndrome [1] [2]. It has been extensively demonstrated both in animals [3] and humans [4] that IH is a determinant of cardiovascular morbidity.…”

Section: Introductionmentioning

confidence: 99%

Intermittent hypoxia-induced delayed cardioprotection is mediated by PKC and triggered by p38 MAP kinase and Erk1/2

Béguin

Belaidi

Godin‐Ribuot

et al. 2007

Journal of Molecular and Cellular Cardiology

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. Intermittent hypoxia-induced delayed cardioprotection is mediated by PKC and triggered by p38 MAP kinase and Erk1/2.. Journal of Molecular and Cellular Cardiology, Elsevier, 2007, 42 (2) AbstractObjective. We previously reported that acute intermittent hypoxia (IH) confers delayed cardioprotection against a prolonged ischemic insult in the rat, via the involvement of nitric oxide synthase and K ATP channels. In the present study, we investigated the role of protein kinase C (PKC), phosphatidylinositol-3-kinase (PI3K), stress activated p38 MAP kinase (MAPK) and extracellular signal regulated kinase (ERK1/2) using selective inhibitors of these pathways. Methods. Adult male rats were exposed to 1-min cycles of IH (10% O 2 , 40 sec) / normoxia (21% O 2 , 20 sec) during 4 hrs or to normoxic cycles. 24 hrs later, isolated hearts were perfused in Langendorff mode and subjected to a 30-min global ischemia followed by 120 min of reperfusion. Results. Compared to normoxic conditions, IH significantly reduced infarct size (22.2  2.4% vs 33.8  2.6%, p<0.05), improved coronary flow and decreased the contracture at reperfusion. When administered before sustained ischemia, chelerythrine (a PKC inhibitor) abolished both the IH-induced reduction in infarct size (36.1  4.9%) and improvement in hemodynamic parameters. In contrast, chelerythrine administration 10 min before IH, did not modify the delayed cardioprotective response. Similarly, wortmannin (a PI3K inhibitor) administration 10 min before IH was unable to block the cardioprotective effects. However, administration of SB203580 (a p38 MAPK inhibitor) and PD98059 (an Erk1/2 inhibitor), 30 min before IH abolished its delayed infarct-sparing effect (32.2  3.4% and 33.9  2.9% respectively). In addition, 24 hrs after IH, a significant increase in p38 MAPK and Erk1/2 phosphorylation was observed by Western blot. Conclusion. These results suggest that the delayed preconditioning induced by intermittent hypoxia does not involve the PI3K signalling pathway and that is mediated by PKC and triggered by p38 MAPK and Erk1/2.

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Invited Review: Physiological and pathophysiological responses to intermittent hypoxia

Cited by 261 publications

References 79 publications

Sleep Oxygen Desaturation Predicts Survival in Idiopathic Pulmonary Fibrosis

Sleep Oxygen Desaturation Predicts Survival in Idiopathic Pulmonary Fibrosis

Invited Review: Neuroplasticity in respiratory motor control

Intermittent hypoxia-induced delayed cardioprotection is mediated by PKC and triggered by p38 MAP kinase and Erk1/2

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