Contributions of hypoxia and respiratory disturbance index to sympathetic activation and blood pressure in obstructive sleep apnea syndrome

Peled, Nir; Greenberg, Avital; Pillar, Giora; Zinder, Oren; Levi, Nurit; Lavie, Peretz

doi:10.1016/s0895-7061(98)00159-9

Cited by 81 publications

(50 citation statements)

References 26 publications

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“…Another possibility that cannot be ignored is that inflammatory/immune activation is modulated by increased sympathetic activation and catecholamine release observed in OSA patients [29]. Sympathetic activation can affect lymphocyte traffic, circulation, proliferation and modulate functional activities [30].…”

Section: Discussionmentioning

confidence: 99%

Activated CD8+ T-lymphocytes in obstructive sleep apnoea

Dyugovskaya

Lavie²,

Hirsh³

et al. 2005

Eur Respir J

106

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T-lymphocytes are implicated in the development of atherosclerosis. The aim of this study was to assess whether the CD8+ T-lymphocytes of obstructive sleep apnoea (OSA) patients undergo phenotypic and functional changes that may exaggerate atherogenic sequelae in OSA.A total of 36 OSA patients, 17 controls and 15 single-night-treated OSA patients were studied. Phenotype and cytotoxicity against K562 target cells were analysed by flow cytometry. Cytotoxicity against human umbilical vein endothelial cells (HUVECs) was assessed by 51 Cr release assay.The cytotoxicity of the CD8+ T-lymphocytes of OSA patients against K562 and HUVECs was significantly greater than controls. This increased cytotoxicity directly depended on the presence of perforin and natural killer receptors (CD56, CD16), which were significantly increased in OSA CD8+ T-lymphocytes. Also the percentage of the CD56bright subset, which mediates initial interactions with vascular endothelium, significantly increased in OSA. Nasal continuous positive airway pressure treatment significantly decreased CD8+ T-cell cytotoxicity and CD56 expression, and was positively correlated with natural killer inhibitory NKB1 receptor expression either after a single-night treatment or after a prolonged treatment.In conclusion, the CD8+ T-lymphocytes of obstructive sleep apnoea patients undergo phenotypic and functional changes, rendering them cytotoxic to target cells via increased CD56+/perforin+ expression, which can be ameliorated by nasal continuous positive airway pressure treatment. These results are compatible with the current authors' hypothesis of atherogenic sequelae in obstructive sleep apnoea.

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Section: Discussionmentioning

confidence: 99%

Activated CD8+ T-lymphocytes in obstructive sleep apnoea

Dyugovskaya

Lavie²,

Hirsh³

et al. 2005

Eur Respir J

106

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show abstract

“…46 The resultant sleep fragmentation and deprivation also induce an increase in cytokines 49 that may underlie inflammatory responses which lead to cardiovascular morbidity.…”

mentioning

confidence: 99%

Serum Inflammatory Markers in Obstructive Sleep Apnea: A Meta-Analysis

Nadeem

Molnár

Madbouly

et al. 2013

Journal of Clinical Sleep Medicine

393

308

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“…9 10 OSA results in repetitive and severe nocturnal hypoxemia and sleep disturbances. 11 The hypoxemia of high altitude results in increases in interleukin-6 (IL-6) 12 and CRP 12,13 in normal humans. Sleep deprivation also induces an increase in cytokines.…”

mentioning

confidence: 99%

Elevated C-Reactive Protein in Patients With Obstructive Sleep Apnea

et al. 2002

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Background-Obstructive sleep apnea (OSA) has been increasingly linked to cardiovascular and cerebrovascular disease.Inflammatory processes associated with OSA may contribute to cardiovascular morbidity in these patients. We tested the hypothesis that OSA patients have increased plasma C-reactive protein (CRP). Methods and Results-We studied 22 patients (18 males and 4 females) with newly diagnosed OSA, who were free of other diseases, had never been treated for OSA, and were taking no medications. We compared CRP measurements in these patients to measurements obtained in 20 control subjects (15 males and 5 females) who were matched for age and body mass index, and in whom occult OSA was excluded. Plasma CRP levels were significantly higher in patients with OSA than in controls (median Epidemiological studies show that an elevated CRP level in the high-normal (0.2 to 1.5 mg/dL) range in apparently healthy men and women is a strong predictor of cardiovascular risk. 7,8 In patients with acute coronary artery disease, stable angina pectoris, and a history of myocardial infarction, higher CRP is also associated with future cardiovascular events. 9 10 OSA results in repetitive and severe nocturnal hypoxemia and sleep disturbances. 11 The hypoxemia of high altitude results in increases in interleukin-6 (IL-6) 12 and CRP 12,13 in normal humans. Sleep deprivation also induces an increase in cytokines. 4,14 We tested the hypothesis that OSA patients have increased plasma CRP. MethodsWe compared subjects with moderate to severe OSA (apnea hypopnea index [AHI] Ն20) to those without OSA (AHI Յ5). We studied 22 patients (18 males and 4 females) with newly diagnosed OSA, who were free of other diseases, had never been treated for OSA, and were taking no medications. We compared CRP measurements in these patients to measurements obtained from 20 control subjects (15 males and 5 females) who were matched for age and body mass index (BMI), and in whom occult OSA was excluded. The control group was free of any acute or chronic cardiovascular, inflammatory, or sleep disorders, and no control subjects were taking medications at the time of the sleep study. The presence and severity of sleep apnea were determined by standard overnight polysomnography, including electroencephalography, electrooculography, electromyography, oximetry, thermistor measurements of airflow, and measurements of rib cage and abdominal movements when breathing. The sleep studies followed a split-night protocol. The first half of the study intended to diagnose OSA, with a therapeutic trial of continuous positive airway pressure during the second half of the night. An apnea was defined as complete cessation of airflow for at least 10 seconds. Hypopnea was defined as a reduction of respiratory signals for at least 10 seconds associated with oxygen desaturation of Ն4%. The AHI was calculated as the total number of respiratory events per hour of sleep.Baseline demographic data, heart rate, blood pressure (SpaceLabs blood pressure monitor 90207), and venous blood ...

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Contributions of hypoxia and respiratory disturbance index to sympathetic activation and blood pressure in obstructive sleep apnea syndrome

Cited by 81 publications

References 26 publications

Activated CD8+ T-lymphocytes in obstructive sleep apnoea

Activated CD8+ T-lymphocytes in obstructive sleep apnoea

Serum Inflammatory Markers in Obstructive Sleep Apnea: A Meta-Analysis

Elevated C-Reactive Protein in Patients With Obstructive Sleep Apnea

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