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Updated: Jul 28, 2026

Drug-Induced Sleep Endoscopy (DISE) with Target Controlled Infusion (TCI) and Bispectral Analysis in Obstructive Sleep Apnea
Published on: December 6, 2016
[Obstructive sleep apnea syndrome: a cardiovascular risk factor?]
H W Duchna1, C Guilleminault, R A Stoohs
1Poliklinik Abteilung für Pneumologie Allergologie und Schlafmedizin Bürkle-de-la-Camp-Platz 1 44789 Bochum, Germany. hans-werner-duchna@ruhr-uni-bochum.de
Obstructive sleep apnea syndrome (OSAS) impairs nitric oxide-mediated vasodilation, a function reversible with continuous positive airway pressure (CPAP) treatment. This suggests endothelial cell dysfunction in OSAS patients.
Area of Science:
- Cardiovascular Medicine
- Sleep Medicine
- Vascular Biology
Background:
- Obstructive sleep apnea syndrome (OSAS) is linked to cardiovascular disease.
- Endothelial dysfunction is a potential mechanism contributing to cardiovascular complications in OSAS.
Purpose of the Study:
- To investigate nitric oxide-mediated vasodilatory function in normotensive OSAS patients.
- To assess both endothelium-dependent and endothelium-independent vasodilation.
Main Methods:
- Utilized the hand vein compliance technique in 23 male OSAS patients and 12 male controls.
- Administered bradykinin (endothelium-dependent) and nitroglycerin (endothelium-independent) to assess vasodilation.
Main Results:
- OSAS patients showed significantly reduced maximum dilation to bradykinin compared to controls.
- Vasodilation to nitroglycerin was not significantly different between groups.
- CPAP treatment in 11 OSAS patients significantly improved bradykinin-induced vasodilation.
Conclusions:
- Endothelium-dependent vasodilation is impaired in OSAS patients, indicating endothelial cell dysfunction.
- This endothelial dysfunction is reversible with CPAP treatment.
- Findings highlight the role of endothelial dysfunction in OSAS-related cardiovascular risks.
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