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Study Objectives: Chronic intermittent hypoxia (CIH) is a major determinant in obstructive sleep apnea cardiovascular morbidity and this effect is influenced by age. The objective of the present study was to assess the differential molecular mechanisms at gene-level expression involved in the cardiovascular remodeling induced by CIH according to chronological age., Methods: Two- and 18-month-old mice (N = 8 each) were subjected to CIH or normoxia for 8 weeks. Total messenger RNA (mRNA) was extracted from left ventricle myocardium and aortic arch, and gene expression of 46 intermediaries of aging, oxidative stress, and inflammation was measured by quantitative real-time polymerase chain reaction., Results: Cardiac gene expression of Nrf2 (2.05-fold increase, p < 0.001), Sod2 (1.9-fold increase, p = 0.035), Igf1r (1.4-fold increase, p = 0.028), Mtor (1.8-fold increase, p = 0.06), Foxo3 (1.5-fold increase, p = 0.020), Sirt4, Sirt6, and Sirt7 (1.3-fold increase, p = 0.012; 1.1-fold change, p = 0.031; 1.3-fold change, p = 0.029) was increased after CIH in young mice, but not in old mice. In aortic tissue, endothelial isoform of nitric oxide synthase was reduced in young mice (p < 0.001), Nrf2 was reduced in 80% (p < 0.001) in young mice and 45% (p = 0.07) in old mice, as its downstream antioxidant target Sod2 (82% reduced, p < 0.001). IL33., Conclusions: CIH effect in gene expression is organ-dependent, and is modulated by age. CIH increased transcriptional expression of genes involved in cardioprotection and cell survival in young, but not in old mice. In aortic tissue, CIH reduced gene expression related to an antioxidant response in both young and old mice, suggesting vascular oxidative stress and a proaging process., (© Sleep Research Society 2021. Published by Oxford University Press on behalf of the Sleep Research Society. All rights reserved. For permissions, please email: journals.permissions@oup.com.)

Background: To improve the performance of simplified sleep studies, it is essential to properly estimate the sleep time., Objectives: Our aim is to estimate sleep efficiency on the basis of flow breathing signal characteristics., Methods: Twenty subjects with sleep apnea-hypopnea syndrome diagnosed by polysomnography were studied. A characteristic pattern of flow signal defined our criteria for wakefulness and sleep. Sleep was analyzed in 2 different runs: (1) in the usual manner (neurological and respiratory variables), and (2) only the nasal cannula flow signal was displayed on the computer screen and the sleep and wakefulness periods were scored according to our criteria. At the end of the scoring process, all the signals were displayed on the screen to analyze the concordance., Results: Three thousand and sixty-nine screens were analyzed. The polysomnography sleep efficiency measured was 80.8%. The estimated sleep efficiency measured by nasal prongs was 78.9%. The detection and concordance of wakefulness had a sensitivity of 58.7%, a specificity of 96.4%, a positive predictive value of 81.3% and a negative predictive value of 89.6%., Conclusions: Our criteria for sleep and wakefulness based on airflow waveform morphology are a helpful parameter for estimating sleep efficiency in a simplified sleep study., (Copyright © 2009 S. Karger AG, Basel.)

Flow limitation during sleep occurs when the rise in esophageal pressure is not accompanied by a flow increase which results in a non-rounded inspiratory flow shape. Short periods of flow limitation ending in an arousal or in a fall in SaO2 (hypopnea or upper airway resistance syndrome) are detrimental but the role of prolonged periods of flow limitation (PPFL) has not yet been clarified. This is important not only for diagnosis but also for nasal continuous positive airway pressure (CPAP) titration, especially for the automatic devices that need to be setup. The aim of this study was to analyze the effects of PPFL. We compared the behavior of the mean end-expiratory systemic blood pressure (SBP), end-tidal CO2, esophageal pressure and the pattern of breathing during a period of normal breathing at optimal (CPAP) and during PPFL at suboptimal CPAP in 14 patients with sleep apnea/hypopnea syndrome during a full polysomnography CPAP titration. The mean values of the parameters studied, at optimal and suboptimal CPAP were (1) SBP 92+/-13 vs. 91+/-15 mmHg (P: ns). At suboptimal CPAP, swings of blood pressure were associated with changes in pleural pressure; (2) SaO2 97.5+/-1.2 vs. 96.5+/-1.6 (P: 0.03), (3) end-tidal CO2 43.5+/-4 vs. 49.5+/-4 (P:0.001); (4) oesophageal pressure, 10.5+/-4 vs. 37.6+/-15 cmH2O (P:0.001) and (5) pattern of breathing: minute ventilation 6.6+/-1.4 vs. 6.1+/-1.2L/min (P: ns) and inspiratory time 1.24+/-0.3 vs. 1.66+/-0.4s (P:0.001). It can be concluded that PPFL induces significant physiological changes. Nevertheless, given the scant literature, clinical studies are warranted to elucidate the clinical role of these physiological changes.