Pharyngeal constrictor muscle fatty change may contribute to obstructive sleep apnea-hypopnea syndrome: a prospective observational study.
Saved in:
| Title: | Pharyngeal constrictor muscle fatty change may contribute to obstructive sleep apnea-hypopnea syndrome: a prospective observational study. |
|---|---|
| Authors: | Shi, Lin (AUTHOR), Wang, Haolin (AUTHOR), Wei, Lai (AUTHOR), Hong, Zhijun (AUTHOR), Wang, Mingyu (AUTHOR), Wang, Zhiqiang (AUTHOR) |
| Source: | Acta Oto-Laryngologica. Dec2016, Vol. 136 Issue 12, p1285-1290. 6p. |
| Subjects: | Biopsy, Histology, Longitudinal method, Obesity, Scientific observation, Research funding, Sleep, Sleep apnea syndromes, Polysomnography, Body mass index, Data analysis software, Descriptive statistics, Pharyngeal muscles, Mann Whitney U Test |
| Abstract: | Conclusions:Pharyngeal constrictor muscle injury and fatty changes may play important roles in the pathogenesis and progression of OSAHS. Objective:Obstructive sleep apnea-hypopnea syndrome (OSAHS) is a respiratory disorder caused by upper airway obstruction during sleep. The primary objectives of this study were to determine the ultrastructural characteristics of the pharyngeal constrictor muscle in patients with OSAHS. Methods:A pharyngeal constrictor muscle specimen was collected from all subjects. The muscle cell ultrastructure was observed under electron microscopy. Results:Eighteen male patients with OSAHS (OSAHS group) and 10 male body mass index-matched patients with chronic tonsillitis (control group) were enrolled in this study. All patients were obese adults. The apnea-hypopnea index (41.22 ± 17.29 vs 2.30 ± 1.10 events/h) was significantly higher and the lowest arterial oxygen saturation (76.00 ± 8.57% vs 97.00 ± 2.00%) was significantly lower in the OSAHS group than in the control group (bothp < 0.001). Myofibril disorder, mitochondrial edema, and intramyocellular lipid droplets were observed in patients with OSAHS. There was a significant correlation between the number of lipid droplets and the apnea-hypopnea index. [ABSTRACT FROM PUBLISHER] |
| Copyright of Acta Oto-Laryngologica is the property of Taylor & Francis Ltd and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.) | |
| Database: | Psychology and Behavioral Sciences Collection |
|
Full text is not displayed to guests.
Login for full access.
|
|
| Abstract: | Conclusions:Pharyngeal constrictor muscle injury and fatty changes may play important roles in the pathogenesis and progression of OSAHS. Objective:Obstructive sleep apnea-hypopnea syndrome (OSAHS) is a respiratory disorder caused by upper airway obstruction during sleep. The primary objectives of this study were to determine the ultrastructural characteristics of the pharyngeal constrictor muscle in patients with OSAHS. Methods:A pharyngeal constrictor muscle specimen was collected from all subjects. The muscle cell ultrastructure was observed under electron microscopy. Results:Eighteen male patients with OSAHS (OSAHS group) and 10 male body mass index-matched patients with chronic tonsillitis (control group) were enrolled in this study. All patients were obese adults. The apnea-hypopnea index (41.22 ± 17.29 vs 2.30 ± 1.10 events/h) was significantly higher and the lowest arterial oxygen saturation (76.00 ± 8.57% vs 97.00 ± 2.00%) was significantly lower in the OSAHS group than in the control group (bothp < 0.001). Myofibril disorder, mitochondrial edema, and intramyocellular lipid droplets were observed in patients with OSAHS. There was a significant correlation between the number of lipid droplets and the apnea-hypopnea index. [ABSTRACT FROM PUBLISHER] |
|---|---|
| ISSN: | 00016489 |
| DOI: | 10.1080/00016489.2016.1205220 |