Effects of Oxygen Administration on the Circulating Vascular Endothelial Growth Factor (VEGF) Levels in Patients with Obstructive Sleep Apnea Syndrome

Teramoto, Shinji; Kume, Haruki; Yamamoto, Hiroshi; Ishii, Takeo; Miyashita, Akira; Matsuse, Takeshi; Akishita, Masahiro; Toba, Kenji; Ouchi, Yasuyoshi

doi:10.2169/internalmedicine.42.681

Cited by 41 publications

(38 citation statements)

References 28 publications

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“…Arterial oxygen saturation (SaO2) was continuously measured via pulse oxymeter (Datex, Helsinki, Finland). Data acquisition was performed overnight starting at 9:00 PM until 7:00 AM the next morning (19,20). Apnea was defined as continuous cessation of airflow for > 10 s, and hypopnea was defined as a reduction in airflow for > 10 s with oxygen desaturation of 4% or an EEG arousal from sleep.…”

Section: Polysomnographymentioning

confidence: 99%

Effect of Nasal Continuous Positive Airway Pressure Treatment on Plasma Adrenomedullin Levels in Patients with Obstructive Sleep Apnea Syndrome: Roles of Nocturnal Hypoxia and Oxidant Stress

Yamamoto¹,

Teramoto²,

Yamaguchi³

et al. 2007

Hypertens Res

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Note from the Editor-in-ChiefDuplicate publication of essentially the same data constitutes a violation of copyright law and of the ethics of scientific publication. When there is doubt about the common source, overlapping, or coincidence of data in articles that are based on the same study, the author(s) must disclose any information about their contribution being under consideration or accepted by another journal at the time of submission of a manuscript. Kazuyuki Shimada Editor-in-Chief Hypertension Research

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Section: Polysomnographymentioning

confidence: 99%

Effect of Nasal Continuous Positive Airway Pressure Treatment on Plasma Adrenomedullin Levels in Patients with Obstructive Sleep Apnea Syndrome: Roles of Nocturnal Hypoxia and Oxidant Stress

Yamamoto¹,

Teramoto²,

Yamaguchi³

et al. 2007

Hypertens Res

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“…Although VEGF has been demonstrated in various types of cells to be stimulated by hypoxia (5), in respiratory diseases with chronic hypoxic manifestation, data about VEGF regulation are conflicting. Several investigations in obstructive sleep apnea (10,15,43,46) and cystic fibrosis (29) revealing an increase in serum VEGF have been criticized, because VEGF is released from activated platelets during the in vitro clotting process (12,17,18). On the other hand, measuring VEGF in plasma (22) and in bronchoalveolar lavage fluid (31) yielded the same result.…”

mentioning

confidence: 99%

Acute hypoxia decreases plasma VEGF concentration in healthy humans

Oltmanns

Gehring

Rudolf

et al. 2006

American Journal of Physiology-Endocrinology and Metabolism

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Vascular endothelial growth factor (VEGF) is known to be upregulated by hypoxia in vitro. However, in vivo data about VEGF regulation in chronic hypoxic diseases are conflicting. We investigated the effects of hypoxia on plasma VEGF concentration in healthy subjects. To control known confounders, such as insulin, glucose concentrations, or exercise, hypoxic effects on VEGF were studied during experimentally clamping glucose concentrations at rest. In a double-blind crossover study design, we induced hypoxia for 30 min by decreasing oxygen saturation to 75% (vs. normoxic control) in 14 healthy men. Plasma VEGF concentration was determined at baseline, immediately after hypoxia had ended, and after a further 150 min. Levels of its soluble (s)Flt-1 receptor were assessed at baseline and at the end of the clamp. In parallel, catecholamine and cortisol levels were monitored. To investigate potential effects of glucose administration on the release of VEGF, we performed a third session, reducing glucose infusion for 30 min while serum insulin was held stable thereby inducing hypoglycemia. Hypoxia decreased VEGF levels compared with the normoxic control ( P < 0.05). VEGF concentrations increased during hypoglycemia ( P < 0.02) but were comparable to the normoglycemic control at the end of the clamp ( P > 0.80). sFlt-1 receptor concentration remained unchanged during hypoxia and hypoglycemia compared with control (both P > 0.4). Epinephrine concentration ( P < 0.01) increased upon hypoxia, whereas norepinephrine and cortisol did not change. Contrary to in vitro studies, in healthy humans hypoxia decreases plasma VEGF concentration, suggesting that systemic VEGF concentration may be differently regulated than the expression on cellular basis.

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“…Activation of redox-sensitive gene expression is suggested by the increase in some protein products of these genes, including VEGF (Teramoto et al, 2003), EPO (Marrone et al, 2008), endothelin-1 (Belaidi et al, 2009), inflammatory cytokines and adhesion molecules (Ohga et al, 1999;Dyugovskaya et al, 2002;Ohga et al, 2003).…”

Section: Oxidative Stressmentioning

confidence: 99%

Obstructive Sleep Apnoea Syndrome as a Systemic Low-Grade Inflammatory Disorder

Zamarrón¹,

Morete²,

Campo³

2012

Cardiovascular Risk Factors

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Effects of Oxygen Administration on the Circulating Vascular Endothelial Growth Factor (VEGF) Levels in Patients with Obstructive Sleep Apnea Syndrome

Abstract: ObjectiveRepeated nocturnal hypoxia is implicated in the pathogenesis of cardiovascular complications in obstructive sleep apnea syndrome (OSAS). Wehypothesized that circulating vascular endothelial growth factor (VEGF)

Cited by 41 publications

References 28 publications

Effect of Nasal Continuous Positive Airway Pressure Treatment on Plasma Adrenomedullin Levels in Patients with Obstructive Sleep Apnea Syndrome: Roles of Nocturnal Hypoxia and Oxidant Stress

Effect of Nasal Continuous Positive Airway Pressure Treatment on Plasma Adrenomedullin Levels in Patients with Obstructive Sleep Apnea Syndrome: Roles of Nocturnal Hypoxia and Oxidant Stress

Acute hypoxia decreases plasma VEGF concentration in healthy humans

Obstructive Sleep Apnoea Syndrome as a Systemic Low-Grade Inflammatory Disorder

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