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Updated: Jun 12, 2026

A Model to Simulate Clinically Relevant Hypoxia in Humans
Published on: December 22, 2016
Choroidal blood-flow responses to hyperoxia and hypercapnia in men with obstructive sleep apnea
Matthieu Tonini1, Hafid Khayi, Jean-Louis Pepin
1Department of Ophthalmology, Grenoble University Hospital, Joseph Fourier University, Grenoble, France.
Study Objectives:
Obstructive sleep apnea (OSA) impacts on macrovasculature and autonomic function and may therefore interfere with ocular microvascular regulation. We hypothesized that choroidal vascular reactivity to hyperoxia and hypercapnia was altered in patients with OSA compared with matched control subjects and would improve after treatment with continuous positive airway pressure (CPAP).
Methods:
Sixteen healthy men were matched 1:1 for body mass index, sex, and age with 16 men with newly diagnosed OSA without comorbidities. Subjects underwent sleep studies, 24-hour blood pressure monitoring, arterial stiffness measurements, and cardiac and carotid echography. Overall, patients were middle-aged, lean, and otherwise healthy except for having OSA with a limited amount of desaturation, with, at most, subclinical lesions of the cardiovascular system, stage 1 hypertension, or both. Choroidal laser Doppler flowmetry provides a unique opportunity to assess microvascular function by measuring velocity, (ChBVel), volume (ChBVol), and relative subfoveal choroidal blood flow (ChBF). Vascular choroidal reactivity was studied during hyperoxia and hypercapnia (8% CO2) challenges before and after treatment with nasal CPAP.
Results:
Patients with OSA and control subjects exhibited similar choroidal reactivity during hyperoxia (stability of choroidal blood flow) and hypercapnia (significant increases in ChBVel of 13.5% and in ChBF of 16%). Choroidal vasoreactivity to CO2 was positively associated with arterial stiffness in patients with OSA. Gas choroidal vasoreactivity was unchanged after 6 to 9 months of CPAP treatment.
Conclusion:
This study showed unimpaired choroidal vascular reactivity in otherwise healthy men with OSA. This suggests that patients with OSA, without comorbidities, have long-term adaptive mechanisms active in ocular microcirculation.
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