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Updated: Jun 5, 2026

A Model to Simulate Clinically Relevant Hypoxia in Humans
Published on: December 22, 2016
Consequences of hypoxia-reoxygenation phenomena in patients with obstructive sleep apnea syndrome
Tansu Ulukavak Ciftci1, Oguz Kokturk, Senay Demirtas
1Sleep Disorders Center, Gazi University Faculty of Medicine, Ankara, Turkey.
Background And Objectives:
Obstructive sleep apnea syndrome (OSAS) is a common disorder characterized by numerous episodes of absence of respiratory flow during sleep, which can be followed by a decrease in SaO2, which is rapidly normalized when ventilation resumes. We hypothesize that this hypoxia-reoxygenation phenomena may affect the generation of vascular endothelial growth factor (VEGF), erythropoietin (EPO), endothelin-1 (ENDO-1), and inducible nitric oxide synthase (iNOS).
Design And Setting:
Prospective, patients referred to sleep disorders center.
Patients And Methods:
The presence and severity of OSAS were determined using the standard overnight polysomnography. Diagnosis of OSAS was made when the apnea-hypopnea index (AHI) was ≥15, independent of the appearance of symptoms. Serum levels of VEGF, EPO, ENDO-1, and nitrite-nitrate were measured after overnight fasting in 69 patients with OSAS and in 17 healthy control subjects. Serum levels of VEGF and nitrite-nitrate were measured again after 12 weeks of treatment with continuous positive airway pressure (CPAP) in OSAS patients.
Results:
Serum VEGF levels were found to be significantly higher and nitrite-nitrate levels were found to be significantly lower in OSAS patients than in controls (P=.003, .008, respectively), but no differences in EPO and ENDO-1 levels were found between the groups. We demonstrated that in OSAS patients, the serum VEGF levels were decreased and nitrate levels were increased after 12 weeks of CPAP treatment (P=.001, .002, respectively).
Conclusion:
According to our data, it is likely that hypoxia-reoxygenation phenomena affect the VEGF and nitrite-nitrate levels, which may be pathogenic factors in generating cardiovascular complications in OSAS.
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