CAJ | 학술논문

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(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<0.01).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.
목적 탐토만성간헐성결양(chronic intermittent hypoxia,CIH)대해설기기전、초미결구급혈청지련소수평적영향,병관찰보충지련소후유무간예효과.방법 건강웅성Wistar대서42지,수궤수자표법분위건강대조조(A조)、만성간헐성결양조(B조)화지련소간예조(C조),매조14지.대B조、C조대서간헐결양(매일8 h,련속5주);동시C조대서급여주사용지련소10μg/차,A조여B조급여무균생리염수0.5 ml/차,경정맥주사,매주2차,지속5주.제5주말채용삽입식쌍겁침전겁인도대서해설기기전,검측각조동물해설기기전전압기선급저양자격화저양자격종지후각시간단평균기전전압;투사전경관찰해설기기세포초미결구적개변.전생리검측후추혈검측지련소수평.결과 B조대서적혈청지련소질량농도(1226.0±112.0)ng/ml((-)x±s,하동)현저저우A조(2491.8±117.9)ng/ml,q=38.2,P<0.01;C조대서적혈청지련소질량농도(1988.3±114.7)ng/ml교B조현저증고(q=23.0,P<0.01).재저양자격전적기선상태시,B조해설기기전전압수평명현저우A조화C조(P치균<0.01);저양자격5 min,A、B、C삼조해설기기전전압교기선시명현증고(P치균<0.01),기증고폭도A조최고,B조최저,C조거중,차이균유통계학의의(P치균<0.01);저양자격종지후적15 min、30 min급45 min,A、C량조해설기전압잉유지재교고적수평,현저고우B조(P치균<0.01).CIH환조성해설기결구적변성,사B조대서기원섬유결구문란,기사용해、소실,선립체수종、척단렬,부분선립체공포개변혹용해소실,이지련소주사조병리개변교경.결론 CIH가인기해설기병리개변급기전활동하강,해변화가능여CIH소치적저지련소혈증유관.
Objective To investigate the effects of chronic intermittent hypoxia (CIH) on electromyograph (EMG) and uhrastructure of geniogloasus (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 adiponeetin treatment (C) groups with 14 rats in each. CIH was performed 8 hours per day for5 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 uhrastrueture 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 among three groups(q_(ab)=17.5;q_(ac)=8.9;q_(bc)=8.6, all P<0.01). 15 min,30 min and45 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, vacuolus 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 ultrastructure of GG, which might be associated with hypoadiponectinemia caused by CIH.