ArticleSleep2022
Temporal changes in coronary artery function and flow velocity reserve in mice exposed to chronic intermittent hypoxia.
Article in Sleep, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 16 citations in OpenAlex.
- Oxygen, carbon dioxide, and nitric oxide: role in the pathophysiology of obstructive sleep apnea.Medical gas research · 2027Review
- Chronic intermittent hypoxia sustains the low-grade inflammatory memory of monocytes via activation of myelopoiesis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Intermittent Hypoxia Mimicking Sleep Apnea Induces Systemic and Tissue Specific Epigenetic Changes and p16-Mediated Cellular Senescence Underlying Vascular Dysfunction.Research square · 2026Article
- Article
- The cardiovascular consequences of chronic sleep fragmentation: Evidence from experimental models of obstructive sleep apnea.Sleep medicine · 2025Article
- Intermittent Hypoxia as a Model of Obstructive Sleep Apnea: Present and Future.Sleep medicine clinics · 2025Review
- On the imperative of including 24-h and longitudinal multidimensional physiological phenotyping in rodent models of sleep apnea.Sleep medicine · 2025Article
- Interactions of Obstructive Sleep Apnea With the Pathophysiology of Cardiovascular Disease, Part 1: JACC State-of-the-Art Review.Journal of the American College of Cardiology · 2024Review
- Chronic intermittent hypoxia facilitates the development of angiotensin II-induced abdominal aortic aneurysm in male mice.Journal of applied physiology (Bethesda, Md. : 1985) · 2024Article
- Links Between Obstructive Sleep Apnea and Myocardial Blood Flow Changes Impacting Adverse Cardiovascular Disease-related Outcomes.Current cardiology reports · 2024Review
- Senolytic-facilitated Reversal of End-Organ Dysfunction in a Murine Model of Obstructive Sleep Apnea.American journal of respiratory and critical care medicine · 2024Article
- Solriamfetol enhances wakefulness and improves cognition and anxiety in a murine model of OSA.Sleep medicine · 2023Article
- ERS International Congress 2022: highlights from the Sleep Disordered Breathing Assembly.ERJ open research · 2023Article
- Cardiovascular Disease in Obstructive Sleep Apnea: Putative Contributions of Mineralocorticoid Receptors.International journal of molecular sciences · 2023Review
- Gut microbiota mediate vascular dysfunction in a murine model of sleep apnoea: effect of probiotics.The European respiratory journal · 2023Article
- Reversing coronary vascular sequelae of intermittent hypoxia: what is the window of opportunity?Sleep · 2022Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
STUDY
objectivesObstructive sleep apnea (OSA) is a chronic condition characterized by intermittent hypoxia (IH) that is implicated in an increased risk of cardiovascular disease (i.e., coronary heart disease, CHD) and associated with increased overall and cardiac-specific mortality. Accordingly, we tested the hypothesis that experimental IH progressively impairs coronary vascular function and in vivo coronary flow reserve.
methodsMale C57BL/6J mice (8-week-old) were exposed to IH (FiO2 21% 90 s-6% 90 s) or room air (RA; 21%) 12 h/day during the light cycle for 2, 6, 16, and 28 weeks. Coronary artery flow velocity reserve (CFVR) was measured at each time point using a Doppler system. After euthanasia, coronary arteries were micro-dissected and mounted on wire myograph to assess reactivity to acetylcholine (ACh) and sodium nitroprusside (SNP).
resultsEndothelium-dependent coronary relaxation to ACh was preserved after 2 weeks of IH (80.6 ± 7.8%) compared to RA (87.8 ± 7.8%, p = 0.23), but was significantly impaired after 6 weeks of IH (58.7 ± 16.2%, p = 0.02). Compared to ACh responses at 6 weeks, endothelial dysfunction was more pronounced in mice exposed to 16 weeks (48.2 ± 5.3%) but did not worsen following 28 weeks of IH (44.8 ± 11.6%). A 2-week normoxic recovery after a 6-week IH exposure reversed the ACh abnormalities. CFVR was significantly reduced after 6 (p = 0.0006) and 28 weeks (p < 0.0001) of IH when compared to controls.
conclusionChronic IH emulating the hypoxia-re-oxygenation cycles of moderate-to-severe OSA promotes coronary artery endothelial dysfunction and CFVR reductions in mice, which progressively worsen until reaching asymptote between 16 and 28 weeks. Normoxic recovery after 6 weeks exposure reverses the vascular abnormalities.
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