Background Obstructive sleep apnea syndrome （OSAS） is an important risk factor for cardiovascular diseases. Chronic intermittent hypoxia （CIH） is considered to be one of the most important causes of cardiovascular diseases in OSA patients. This repeated hypoxia and reoxygenation cycle is similar to hypoxia-reperfusion injury, which initiates oxidative stress. In this study, we observed cardiocytes injury induced by CIH and the effect of N-acetylcysteine （NAC）. Methods Thirty ICR mice were randomly assigned to 3 groups： control, CIH and NAC （CIH＋NAC） groups. Malondialdehyde （MDA） and superoxide dismutase （SOD） of cardiocyte homogenates were measured. Serum lipids were measured by an instrument method. Serum cardiac troponin I （cTnl） was detected by enzyme-linked immunosorbent assays （ELISA）. Myocardium pathological sections were observed. Results （1） The SOD activity and MDA concentration of cardiocyte homogenates in the CIH group were significantly higher than in other groups （P 〈0.005）. The MDA concentration of the NAC group was lower than that of the control group （P 〈0.01）. （2） The serum cTnl concentration of the CIH and NAC groups was significantly higher than that of the control group （P 〈0.01）. （3） Serum triglyceride levels in the NAC group were lower than in the other groups （P 〈0.01）, while there were no significant differences in low density lipoprotein and high density lipoprotein among the three groups. （4） The degeneration of myocardium, transverse striation blurred, and fabric effusion were observed in tissue sections in the CIH and NAC groups. However, normal tissue was found in the control group. Conclusion The oxidative stress induced by CIH can injure cardiocytes and the injury effect can be partially inhibited by NAC.
LIU Jian-nanZHANG Jie-xinLU ganQIU YanYANG DiYIN Guo-yongZHANG Xi-long
Background The 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.Methods Forty-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 μg 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.Results CIH 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.Conclusion CIH 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 ClH.
