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A Novel Model of Obstructive Sleep Apnea for Studying Cardiovascular Disease
Author(s) -
Heintz Timothy,
Lux Jacob,
McLerie Meredith,
Durgan David J,
Panama Brian K
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.lb606
Subject(s) - medicine , obstructive sleep apnea , cardiology , apnea , airway , ventricular fibrillation , sleep (system call) , anesthesia , balloon , computer science , operating system
Background Obstructive sleep apnea (OSA) is associated with cardiovascular disease. OSA is characterized by transient upper airway closures during sleep (apneas), and up to 24% of adults in the United States have OSA, many of whom are unaware of their condition. Patients with OSA exhibit daytime sleepiness, may have mood disorders, and are at increased risk for arrhythmias, such as a trial fibrillation. Despite the association between OSA and cardiac disease the specific mechanisms remain elusive. We have initiated a recently developed novel rat model of OSA which closely recapitulates the human condition by incorporating true apneas. Our goal was to examine the effects of OSA on several genes associated with cardiac fibrosis. Methods and Results To generate our OSA model, a silicone balloon was surgically implanted in the trachea of a rat (aged 45–70 days). To produce apneas, the balloon was inflated to transiently obstruct the airway. Unanesthetized, freely‐ranging rats were randomly given sixty 10‐second obstructions (apneas) per hour during their sleep phase (09:00–17:00) for 14 days. Control rats had obstruction devices implanted but the balloons were not inflated. Balloon inflations caused decreases in O 2 saturations in OSA rats from 95.6±0.2% to 74.8±1.2%, and there were no differences in O 2 saturations when balloons were deflated. O 2 saturation decreases caused by apneas were also consistent throughout the experimental period. Measurements of mRNA from the ventricles after two weeks of OSA showed 2‐fold increases in the inflammatory cytokines TNF‐α and TGFβ‐2. Conclusions OSA is associated with increased cardiac expression of genes implicated in cardiac pathology. Our data demonstrates the utility of this novel rat model to study OSA‐induced cardiac disease.