Abstract
The aim of this study was to investigate the effects of mandibular advancement device (MAD) therapy for obstructive sleep apnea–hypopnea syndrome (OSAHS) on hypoxia-inducible factor-1α (HIF-1α), erythropoietin (EPO) and vascular endothelial growth factor (VEGF) in myocardial tissue. New Zealand rabbits were used to develop OSAHS and MAD models. Cone beam computed tomography (CBCT) of the upper airway and polysomnography (PSG) recordings were performed with the animals in the supine position. All of the animals were induced to sleep in a supine position for 4–6 h each day and were observed continuously for 8 weeks. The myocardial tissue of the three groups was dissected to measure the expression of HIF-1α, EPO and VEGF. The results showed that there was higher expression of HIF-1α, EPO and VEGF in the OSAHS group than those in the MAD and control groups. MAD treatment significantly downregulated the expression of HIF-1α, EPO and VEGF in the OSAHS animals. We concluded that MAD treatment could significantly downregulate the increased expression of HIF-1α, EPO and VEGF in OSAHS rabbits, improving their myocardial function.
Highlights
Obstructive sleep apnea–hypopnea syndrome (OSAHS) is an increasingly common public health problem, with a prevalence of 9% of the middle-aged male population and 4% of the female population[1]
obstructive sleep apnea–hypopnea syndrome (OSAHS)‐like clinical symptoms could be relieved by Mandibular advancement devices (MAD) treatment
Sleep respiration in the MAD group was basically uniform, and the above OSAHS-like symptoms were significantly reduced, which suggested that the MADs could relieve clinical symptoms induced by upper airway obstruction
Summary
Obstructive sleep apnea–hypopnea syndrome (OSAHS) is an increasingly common public health problem, with a prevalence of 9% of the middle-aged male population and 4% of the female population[1]. Erythropoietin (EPO) and vascular endothelial growth factor (VEGF), the downstream factors of HIF-1α, are involved in erythropoiesis, angiogenesis, the regulation of extracellular matrix and apoptosis, affecting cardiac function and morphology[6,7,8,9]. Little is known about the changes in HIF-1α, EPO and VEGF in the myocardium of OSAHS patients. Most studies have focused on the changes in the subjective symptoms and airway size of OSAHS patients after MAD treatment. This study was designed to evaluate the changes of HIF-1α, EPO and VEGF in the myocardium of OSAHS animal models we developed previously[12] and to further investigate the effects of MAD treatment on these changes, providing evidence to guide clinical treatment
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