中华物理医学与康复杂志
中華物理醫學與康複雜誌
중화물리의학여강복잡지
CHINESE JOURNAL OF PHYSICAL MEDICINE AND REHABILITATION
2013年
8期
603-608
,共6页
张晓雷%迟永辉%侯晓丽%庞宝森
張曉雷%遲永輝%侯曉麗%龐寶森
장효뢰%지영휘%후효려%방보삼
肺气肿%外周骨骼肌%病理形态学%生物力学%氧化代谢
肺氣腫%外週骨骼肌%病理形態學%生物力學%氧化代謝
폐기종%외주골격기%병리형태학%생물역학%양화대사
Emphysema%Peripheral skeletal muscle%Pathomorphology%Biomechanics%Oxidative metabolism
目的 观察肺气肿对大鼠外周骨骼肌生物力学、病理形态学及氧化代谢功能的影响.方法 采用随机数字表法将20只SD大鼠分为肺气肿组及对照组.通过向气管内滴注猪胰弹性蛋白酶将肺气肿组大鼠制作肺气肿动物模型,对照组大鼠则于相同时间点向气管内滴注生理盐水.于滴药后第20周时行大鼠原位腓肠肌生物力学测定,并检测肌纤维组分构成、毛细血管密度、肌细胞内脂褐素包涵体含量(LI/F)、一氧化氮合酶(NOS)在腓肠肌中的表达及肌肉组织匀浆中氧化代谢酶活性变化.结果 肺气肿组大鼠腓肠肌抗疲劳耐力降低,肌力半数恢复时间[(145.0±55.4)s]较对照组[(55.2±29.3)s]延长(P<0.05),I型肌纤维比例[(16.0±5.0)%]较对照组[(30.7±4.1)%]降低(P<0.05),Ⅱb/x型肌纤维比例[(27.3±4.8)%]较对照组[(11.0±3.2)%]增高(P<0.05);毛细血管密度[(513.9±71.1)n/mm2]较对照组[(578.6±59.9) n/mm2]降低(P<0.05);腓肠肌脂褐素包涵体含量(3.3±0.5)较对照组(1.7±0.4)增高(P<0.05);腓肠肌组织中内皮细胞型NOS(eNOS)表达(1.9±0.5)较对照组(3.4±0.6)降低(P<0.05),神经元型NOS(nNOS)表达与对照组间差异无统计学意义(P>0.05),诱导型NOS(iNOS)在2组大鼠腓肠肌中均未见发现.结论 肺气肿可导致大鼠外周骨骼肌生物力学、病理形态学及氧化代谢功能发生异常改变.
目的 觀察肺氣腫對大鼠外週骨骼肌生物力學、病理形態學及氧化代謝功能的影響.方法 採用隨機數字錶法將20隻SD大鼠分為肺氣腫組及對照組.通過嚮氣管內滴註豬胰彈性蛋白酶將肺氣腫組大鼠製作肺氣腫動物模型,對照組大鼠則于相同時間點嚮氣管內滴註生理鹽水.于滴藥後第20週時行大鼠原位腓腸肌生物力學測定,併檢測肌纖維組分構成、毛細血管密度、肌細胞內脂褐素包涵體含量(LI/F)、一氧化氮閤酶(NOS)在腓腸肌中的錶達及肌肉組織勻漿中氧化代謝酶活性變化.結果 肺氣腫組大鼠腓腸肌抗疲勞耐力降低,肌力半數恢複時間[(145.0±55.4)s]較對照組[(55.2±29.3)s]延長(P<0.05),I型肌纖維比例[(16.0±5.0)%]較對照組[(30.7±4.1)%]降低(P<0.05),Ⅱb/x型肌纖維比例[(27.3±4.8)%]較對照組[(11.0±3.2)%]增高(P<0.05);毛細血管密度[(513.9±71.1)n/mm2]較對照組[(578.6±59.9) n/mm2]降低(P<0.05);腓腸肌脂褐素包涵體含量(3.3±0.5)較對照組(1.7±0.4)增高(P<0.05);腓腸肌組織中內皮細胞型NOS(eNOS)錶達(1.9±0.5)較對照組(3.4±0.6)降低(P<0.05),神經元型NOS(nNOS)錶達與對照組間差異無統計學意義(P>0.05),誘導型NOS(iNOS)在2組大鼠腓腸肌中均未見髮現.結論 肺氣腫可導緻大鼠外週骨骼肌生物力學、病理形態學及氧化代謝功能髮生異常改變.
목적 관찰폐기종대대서외주골격기생물역학、병리형태학급양화대사공능적영향.방법 채용수궤수자표법장20지SD대서분위폐기종조급대조조.통과향기관내적주저이탄성단백매장폐기종조대서제작폐기종동물모형,대조조대서칙우상동시간점향기관내적주생리염수.우적약후제20주시행대서원위비장기생물역학측정,병검측기섬유조분구성、모세혈관밀도、기세포내지갈소포함체함량(LI/F)、일양화담합매(NOS)재비장기중적표체급기육조직균장중양화대사매활성변화.결과 폐기종조대서비장기항피로내력강저,기력반수회복시간[(145.0±55.4)s]교대조조[(55.2±29.3)s]연장(P<0.05),I형기섬유비례[(16.0±5.0)%]교대조조[(30.7±4.1)%]강저(P<0.05),Ⅱb/x형기섬유비례[(27.3±4.8)%]교대조조[(11.0±3.2)%]증고(P<0.05);모세혈관밀도[(513.9±71.1)n/mm2]교대조조[(578.6±59.9) n/mm2]강저(P<0.05);비장기지갈소포함체함량(3.3±0.5)교대조조(1.7±0.4)증고(P<0.05);비장기조직중내피세포형NOS(eNOS)표체(1.9±0.5)교대조조(3.4±0.6)강저(P<0.05),신경원형NOS(nNOS)표체여대조조간차이무통계학의의(P>0.05),유도형NOS(iNOS)재2조대서비장기중균미견발현.결론 폐기종가도치대서외주골격기생물역학、병리형태학급양화대사공능발생이상개변.
Ohjective To study the effects of emphysema on peripheral skeletal muscle biomechanics,pathomorphology and oxidative metabolism in rats.Methods Twenty Sprague-Dawley rats were used and randomized equally into a control group and an emphysema group.A dose of 40 U/100 g body weight of porcine pancreatic elastase was instilled into the trachea of the animals of the emphysema group to model emphysema,while the same volume of saline was instilled into those of the control group.Twenty weeks after instillation,in situ mechanical properties of gastrocnemius were evaluated.Gastrocnemius fiber type composition and capillary density (CD) were assessed by using ATPase staining.Lipofuscin accumulation (LI/F) was determined with the ferric-ferricyanide reduction test technique.Immunohistochemistry was used for the detection of nitric oxide synthases (NOS) in gastrocnemius.The muscle biopsy homogenate was used to measure the activity of superoxide dismutase (SOD),catalase (CAT),NOS,total antioxidant capacity (T-AOC) and the content of nitric oxide (NO).Results Emphysema increased fatigability and decreased the recovery rate of gastrocnemius muscle [(145.0 ± 55.4) s vs (55.2 ± 29.3)s,P < 0.05].Compared to control,the gastrocnemius muscle in rats with emphysema had a lower CD [(513.9±71.1)n/mm2 vs (578.6 ±59.9)n/mm2,P <0.05] and a decreased proportion of type I fibers [(16.0 ±5.0)% vs (30.7 ±4.1) %,P <0.05],with a reciprocal increase in type II b/x fibers [(27.3 ±4.8)%vs (11.0±3.2)%,P<0.05].LI/F was higher (3.3±0.5 vsl.7±0.4,P<0.05) and the activity of SOD,CAT and T-AOC was increased in emphysema group.Compared with control,rats with emphysema demonstrated a lower expression of endothelial NOS (eNOS) (1.9 ± 0.5 vs 3.4 ± 0.6,P < 0.05),and an equivalent expression of neuronal NOS (nNOS) (4.7 ± 1.0 vs 5.1 ± 0.8,P > 0.05) in the gastrocnemius muscle.The inducible NOS (iNOS) was not found in both groups.Conclusions Emphysema could induce biomechanical,pathomorphological and oxidative metabolic changes in peripheral skeletal muscle.