慢性间歇性缺氧对颏舌肌的影响及脂联素干预的探索
本文选题:睡眠呼吸暂停 切入点:阻塞性 出处:《南京医科大学》2010年硕士论文 论文类型:学位论文
【摘要】: 目的探讨慢性间歇性缺氧(chronic intermittent 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8 h,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0.5 ml/次,颈静脉注射,每周2次,持续5周。第6周初采用插入式双极针电极引导大鼠颏舌肌肌电,检测各组动物在低氧刺激前、低氧刺激和低氧刺激终止后各时间段的颏舌肌平均肌电电压;以透射电镜观察颏舌肌肌细胞超微结构的改变。 结果B组大鼠的血清脂联素质量浓度(1226.0±112.0) ng/ml显著低于A组(2491.8±117.9)ng/ml,(q=38.2,P0.01);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,P0.01)。在低氧刺激前的基线状态时,B组颏舌肌肌电电压水平(81.3±9.4)μV明显低于A组(105.4±11.3)μV和C组(98.8±10.9)μV (q值分别为8.0、5.8,P值均0.01);低氧刺激5 min,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(qab=17.5;qac=8.9;qbc=8.6,P值均0.01);低氧刺激终止后的15 min、30 min及45 min,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0.001)。CIH还造成颏舌肌结构的变性如肌原纤维结构紊乱,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,而脂联素可在一定程度上减轻这些病理改变。 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。
[Abstract]:Objective to investigate the effects of chronic intermittent hypoxia (intermittent) on genioglossus myoelectricity, ultrastructure and serum adiponectin levels, and to observe the effect of adiponectin supplementation. Methods 42 healthy male Wistar rats were used. Randomly divided into healthy control group A group, chronic intermittent hypoxia group B group) and adiponectin intervention group with 14 rats in each group. Rats in group B were subjected to intermittent hypoxia (8 hours per day for 5 weeks), while rats in group C were given intermittent hypoxia for 5 weeks. Adiponectin 10 渭 g / time group A and group B were given aseptic saline for 0.5 ml/. At the beginning of the sixth week, the genioglossus electromyography was guided by inserted bipolar needle electrode, and the genioglossus myoelectric activity was detected before hypoxia stimulation. The mean electromyoelectric voltage of genioglossus muscle was observed by transmission electron microscope and the ultrastructure of genioglossus muscle cells was observed by transmission electron microscope. Results the serum lipid diathesis concentration (1226.0 卤112.0) ng/ml in group B was significantly lower than that in group A (2491.8 卤117.9ng / ml). The serum lipid diathesis concentration in group C was significantly higher than that in group C (1988.3 卤114.7ng / ml vs B). The electromyoelectric voltages of genioglossus in group B were significantly higher than those in group B before hypoxia. The Q values of the genioglossus in group A were significantly lower than those in group A (105.4 卤11.3) 渭 V and in group C (98.8 卤10.9) 渭 V (P = 0.01), respectively, and the electromyoelectric voltage of genioglossus in group C was significantly higher than that in group A (P = 0.01) after 5 min hypoxia stimulation, and the median value in group A was the highest in group A and the lowest in group B (P < 0.05). The difference was statistically significant (P < 0.01), and the voltage of genioglossus in groups 15 to 30 min and 45 min after hypoxia was still high, which was significantly higher than that in group B (P = 0.001.CIH), and it also caused the degeneration of genioglossus muscle structure such as myofibrillar structure disorder, which was significantly higher than that in group B (P = 0.001. CIH), and was significantly higher than that in group B (P = 0.001. CIH). Myofilament dissolved, disappeared, mitochondria edema, cristal rupture, partial mitochondrial vacuolation or dissolution disappeared, but adiponectin could alleviate these pathological changes to some extent. Conclusion CIH can induce the pathological changes and the decrease of myoelectric activity in genioglossus, which may be related to hypoadiponectinemia induced by CIH.
【学位授予单位】:南京医科大学
【学位级别】:硕士
【学位授予年份】:2010
【分类号】:R766
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