慢性间歇性缺氧对颏舌肌的影响及脂联素干预的探讨

Effect of chronic intermittent hypoxia on genioglossus and its intervention by adiponectin

目的探讨慢性间歇性缺氧（chronicinterm ittent hypoxia，CIH）对颏舌肌肌电、超微结构及血清脂联素水平的影响，并观察补充脂联素后有无干预效果。方法健康雄性Wistar大鼠42只，随机数字表法分为健康对照组（A组）、慢性间歇性缺氧组（B组）和脂联素干预组（C组），每组14只。对B组、C组大鼠间歇缺氧（每日8h，连续5周）；同时C组大鼠给予注射用脂联素10μg/次，A组与B组给予无菌生理盐水0．5ml／次，颈静脉注射，每周2次，持续5周。第5周末采用插入式双极针电极引导大鼠颏舌肌肌电，检测各组动物颏舌肌肌电电压基线及低氧刺激和低氧刺激终止后各时间段平均肌电电压；透射电镜观察颏舌肌肌细胞超微结构的改变。电生理检测后抽血检测脂联素水平。结果B组大鼠的血清脂联素质量浓度（1226．0±112．0）ng／ml（x±s，下同）显著低于A组（2491．8±117．9）ng／ml，q=38．2，P〈0．01；C组大鼠的血清脂联素质量浓度（1988．3±114．7）ng／ml较B组显著增高（q=23．0，P〈0．01）。在低氧刺激前的基线状态时，B组颏舌肌肌电电压水平明显低于A组和C组（P值均〈0．01）；低氧刺激5min，A、B、C三组颏舌肌肌电电压较基线时明显增高（P值均〈0．01），其增高幅度A组最高，B组最低，C组居中，差异均有统计学意义（P值均〈0．01）；低氧刺激终止后的15min、30min及45min，A、C两组颏舌肌电压仍维持在较高的水平，显著高于B组（P值均〈0．01）。CIH还造成颏舌肌结构的变性，使B组大鼠肌原纤维结构紊乱，肌丝溶解、消失，线粒体水肿、嵴断裂，部分线粒体空泡改变或溶解消失，而脂联素注射组病理改变较轻。结论CIH可引起颏舌肌病理改变及肌电活动下降，该变化可能与CIH所致的低脂联素血症有关。

Objective To investigate the effects of chronic intermittent hypoxia （CIH） on electromyograph （EMG） and uhrastructure of genioglossus （GG） and the interventive effects with adiponectin supplement. Methods 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 10μg 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. Results 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 amonce three groups （ qab = 17.5 ;qac = 8.9 ;qbc = 8.6, all P 〈 0.01 ）. 15 min,30 rain 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, vaeuolus and lysis of some mitochondria in group B. Venous supplement of adiponectin could improve pathological changes resulting from CIH. Conclusions CIH could resulted in pathological changes in EMG and ultrastrueture of GG, which might be associated with hypoadiponectinemia caused by CIH.