Shen Jiu-Cheng, Zhang Xi-Long, Li Chong
Department of Respiratory Medicine of the First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Zhonghua Er Bi Yan Hou Tou Jing Wai Ke Za Zhi. 2009 Oct;44(10):837-42.
To investigate the effects of chronic intermittent hypoxia (CIH) on electromyograph (EMG) and ultrastructure of genioglossus (GG) and the interventive effects with adiponectin supplement.
Forty-two healthy male Wistar rats were randomly divided into normal control (A), CIH (B) and adiponectin treatment (C) groups with 14 rats in each. CIH was performed 8 hours per day for 5 weeks in both group B and C. In group C, transvenous injection of adiponectin of 10 microg dosage each time, twice a week for 5 weeks. While in group A and B, transvenous injection of saline was performed twice a week for 5 weeks. At the beginning of 6th week the GG EMG voltages were measured before, during and following hypoxia stimulation by inserted bipolar needle electrodes and compared among three groups. Transmission electron microscope was used for observation of ultrastructure of GG.
The serum adiponectin level in group B (1226.0 +/- 112.0) ng/ml (x(-) +/- s) was significantly lower than that in group A (2491.8 +/- 117.9) ng/ml, q = 38.2, P < 0.01), and adiponectin level in group C (1988.3 +/- 114.7) ng/ml was significantly higher than that in group B (q = 23.0, P < 0.01). Comparison of GG EMG activity showed that the baseline amplitude of GG EMG before hypoxia stimulation was significantly lower in group B than that in both group A and group C (all P < 0.01). At the 5th min of hypoxia stimulation the GG EMG activities were significantly enhanced among three groups (all P < 0.01). Such an enhancement was the most evident in group A but the least remarkable in group B, with a significant difference among three groups (q(ab) = 17.5; q(ac) = 8.9; q(bc) = 8.6, all P < 0.01). 15 min, 30 min and 45 min after hypoxia stimulation the amplitude of GG EMG remained at relative higher levels in group A and C, significantly higher than that in group B (all P < 0.01). CIH could cause significant ultrastructural pathological changes such as myofibril discontinuities, lysis of myofilament, edema of mitochondria and disruption of cristae, vacuoles and lysis of some mitochondria in group B. Venous supplement of adiponectin could improve pathological changes resulting from CIH.
CIH could resulted in pathological changes in EMG and ultrastructure of GG, which might be associated with hypoadiponectinemia caused by CIH.
探讨慢性间歇性缺氧（CIH）对舌肌（GG）肌电图（EMG）及超微结构的影响以及脂联素补充的干预作用。
42只健康雄性Wistar大鼠随机分为正常对照组（A组）、CIH组（B组）和脂联素治疗组（C组），每组14只。B组和C组每天进行8小时的CIH处理，持续5周。C组经静脉每次注射10μg脂联素，每周2次，共5周。而A组和B组经静脉每周注射2次生理盐水，共5周。在第6周开始时，通过插入双极针电极在缺氧刺激前、刺激期间和刺激后测量GG的EMG电压，并在三组之间进行比较。采用透射电子显微镜观察GG的超微结构。
B组血清脂联素水平为（1226.0±112.0）ng/ml（x(-)±s），显著低于A组（2491.8±117.9）ng/ml，q = 38.2，P < 0.01），C组脂联素水平（1988.3±114.7）ng/ml显著高于B组（q = 23.0，P < 0.01）。GG的EMG活性比较显示，缺氧刺激前GG的EMG基线振幅在B组显著低于A组和C组（均P < 0.01）。在缺氧刺激第5分钟时，三组GG的EMG活性均显著增强（均P < 0.01）。这种增强在A组最明显，在B组最不显著，三组之间有显著差异（q(ab)=17.5；q(ac)=8.9；q(bc)=8.6，均P < 0.01）。缺氧刺激后15分钟、30分钟和45分钟，A组和C组GG的EMG振幅保持在相对较高水平，显著高于B组（均P < 0.01）。CIH可导致显著的超微结构病理改变，如B组出现肌原纤维连续性中断、肌丝溶解、线粒体水肿和嵴断裂、一些线粒体空泡化和溶解。静脉补充脂联素可改善CIH引起的病理改变。
CIH可导致GG的EMG和超微结构发生病理改变，这可能与CIH引起的低脂联素血症有关。
