Changes in genioglossus and their association with serum adiponectin levels in rats subjected to chronic intermittent hypoxia.
- Author:
Xiao-feng ZHANG
1
;
Ya-hui WANG
;
Qin LI
;
Xi-long ZHANG
;
Jiu-cheng SHEN
;
Chong LI
;
Hao LIU
Author Information
- Publication Type:Journal Article
- MeSH: Adiponectin; administration & dosage; blood; Animals; Electromyography; Hypoxia; blood; physiopathology; Male; Microscopy, Electron, Transmission; Muscle, Skeletal; physiology; ultrastructure; Random Allocation; Rats; Rats, Wistar; Sleep Apnea, Obstructive; blood; physiopathology; Tongue; physiology; ultrastructure
- From: Chinese Medical Journal 2010;123(16):2249-2253
- CountryChina
- Language:English
-
Abstract:
BACKGROUNDThe genioglossus (GG) is involved in the maintenance of an open airway for effective breathing. Although the pathogenesis of obstructive sleep apnea hypopnea syndrome (OSAHS) was closely associated with GG dysfunction, its causes and possible treatment have not been elucidated. The aim of the study was to investigate the effects of chronic intermittent hypoxia (CIH) on serum adiponectin levels, electromyograph (EMG) activity and ultrastructure of GG, as well as the effect of an adiponectin supplement in anesthetized rats.
METHODSForty-two healthy male Wistar rats were randomly divided into normal control (A), CIH (B) and adiponectin treatment (C) groups, 14 rats in each group. CIH was performed eight hours per day for five weeks in both groups B and C. Group C received transvenous injection of adiponectin at the dosage of 10 microg per injection, twice a week for five weeks. At the end of the 5th week the GG EMG voltage was measured and compared among the three groups. Transmission electron microscope was used to observe the ultrastructure of the GG.
RESULTSCIH caused significant hypoadiponectinemia, weakened activity of GG EMG at both baseline and hypoxia stimulation, and induced ultrastructural pathological changes, such as, myofibril discontinuities, lysis of myofilament, edema of mitochondria and disruption of cristae, vacuolus and lysis of some mitochondria. Venous supplement of adiponectin improved the above pathological changes resulting from CIH.
CONCLUSIONCIH resulted in pathological changes in GG's EMG and ultrastructure, which could be improved by supplement of adiponectin and be associated with hypoadiponectinemia caused by CIH.