CAJ | 학술논문

背景:组织毛细血管增多,可缩短氧从毛细血管向组织细胞弥散的距离,改善组织供氧.但组织毛细血管密度与组织的代谢水平密切相关,单纯缺氧能否引起骨骼肌毛细血管密度增加尚有争议.目的:观察不同缺氧时间大鼠骨骼肌毛细血管密度和血流供应的变化规律.设计:非随机对照实验.对动物缺氧前体质量加以选择,使各组动物的体质量在缺氧末期基本接近.地点和对象:实验地点:第三军医大学病理生理学与高原生理学教研室.清洁级纯种健康Wistar大鼠64只,雌雄各半,分为4组:对照组、缺氧5 d组、缺氧15 d组和缺氧30 d组.干预:缺氧5 d组、15 d组和30 d组大鼠在模拟海拔5 000 m的减压舱中分别连续减压缺氧5,15和30 d后(23 h/d),对照组大鼠在舱外饲养.用肌球蛋白ATP酶(mATPase)组织化学方法显示骨骼肌Ⅰ,Ⅱ型纤维和毛细血管并进行图像分析,测定骨骼肌纤维横断面积和毛细血管密度以及单位面积内毛细血管数与肌纤维数的比值;用放射性微球法测定骨骼肌血流量和血管阻力.主要观察指标:①各组大鼠血球压积和骨骼肌血流量、血管阻力的变化.②大鼠腓肠肌Ⅰ,Ⅱ型纤维横断面积.③各组大鼠骨骼肌毛细血管密度和单位面积内毛细血管数与肌纤维数的比值.结果:缺氧5 d组大鼠与对照组相比,骨骼肌纤维横断面积即出现显著缩小[I型分别为(2 254±298),(2 947±235)μm2;Ⅱ型分别为(1 609±339),(2 391±223)μm2],15 d和30d组大鼠毛细血管密度分别为(657±35)/mⅡ2和(661±50)/mm2,与对照组[(599±42)/mm2]相比显著增高,但单位面积内毛细血管数/肌纤维数的比值无明显变化.在所观测的时间内,各组大鼠骨骼肌血流量和血管阻力未见明显变化.结论:单纯缺氧大鼠骨骼肌毛细血管并未发生真正增生,但缺氧引起的骨骼肌纤维萎缩,可使毛细血管密度相对增多.
배경:조직모세혈관증다,가축단양종모세혈관향조직세포미산적거리,개선조직공양.단조직모세혈관밀도여조직적대사수평밀절상관,단순결양능부인기골격기모세혈관밀도증가상유쟁의.목적:관찰불동결양시간대서골격기모세혈관밀도화혈류공응적변화규률.설계:비수궤대조실험.대동물결양전체질량가이선택,사각조동물적체질량재결양말기기본접근.지점화대상:실험지점:제삼군의대학병리생이학여고원생이학교연실.청길급순충건강Wistar대서64지,자웅각반,분위4조:대조조、결양5 d조、결양15 d조화결양30 d조.간예:결양5 d조、15 d조화30 d조대서재모의해발5 000 m적감압창중분별련속감압결양5,15화30 d후(23 h/d),대조조대서재창외사양.용기구단백ATP매(mATPase)조직화학방법현시골격기Ⅰ,Ⅱ형섬유화모세혈관병진행도상분석,측정골격기섬유횡단면적화모세혈관밀도이급단위면적내모세혈관수여기섬유수적비치;용방사성미구법측정골격기혈류량화혈관조력.주요관찰지표:①각조대서혈구압적화골격기혈류량、혈관조력적변화.②대서비장기Ⅰ,Ⅱ형섬유횡단면적.③각조대서골격기모세혈관밀도화단위면적내모세혈관수여기섬유수적비치.결과:결양5 d조대서여대조조상비,골격기섬유횡단면적즉출현현저축소[I형분별위(2 254±298),(2 947±235)μm2;Ⅱ형분별위(1 609±339),(2 391±223)μm2],15 d화30d조대서모세혈관밀도분별위(657±35)/mⅡ2화(661±50)/mm2,여대조조[(599±42)/mm2]상비현저증고,단단위면적내모세혈관수/기섬유수적비치무명현변화.재소관측적시간내,각조대서골격기혈류량화혈관조력미견명현변화.결론:단순결양대서골격기모세혈관병미발생진정증생,단결양인기적골격기섬유위축,가사모세혈관밀도상대증다.
BACKGROUND: The increase of blood capillaries in tissues can shorten the distance of oxygen diffusion from blood capillary to tissue cells and ameliorate oxygen supplement in tissues. However, capillary density is closely related to metabolic level of tissues, so it is still controversial whether mere hypoxia can induce the increase of capillary density in skeletal muscle.OBJECTIVE: To observe the changing regulations of capillary density of skeletal muscle and blood flow in rats at different time points of hypoxia.DESIGN: A non-randomized and controlled experiment. Body mass of animals before hypoxia was selected in order to achieve similar body mass of them at the end of hypoxia.SETTING and PARTICIPANTS: The experiment was completed in the Department of Pathophysiology and Institute of High Altitude Medicine,Third Military Medical University of Chinese PLA. A total of 64 Wistar rats,half male and half female, were divided into 4 groups: control group,5-day, 15-day and 30-day hypoxia group.INTERVENTIONS: Rats in the 5-day, 15-day and 30-day hypoxia group were kept in a large hypobaric chamber with a simulated elevation of 5 000 m for 5 days, 15 days and 30 days respectively(23 hours per day). Rats in the control group were kept under normobaric condition. Myosin-ATPase (mATPase) histochemistry was used to display type Ⅰ and Ⅱ fiber of skeletal muscle and blood capillary, and imaging analysis was carried out. It was also used to assay the fiber cross-sectional area(FCSA) of skeletal muscle,capillary density(CD) and ratio of capillary number/fiber number(C/F) in a unit area. Radioactive biomicrosphere method was used to assay blood flow and vascular resistance of skeletal muscle.capillary number/fiber number(C/F) in a unit area of rats in all groups.RESULTS: FCSA of skeletal muscle was significantly decreased of rats in the 5 -day hypoxia group [typeⅠwas (2254±298), (2947±235) μm2 respectively; type Ⅱ was (1 609 + 339) , (2 391 ± 223) μm2 respectively];CD of rats in the 15-day and 30 day hypoxia group was(657 +35)/mm2and(661±50)/mm2, which were significantly higher than that in the control group[(599 ±42)/mm2], but the ratio of C/F remained unchanged significantly. There was no obvious change in blood flow supply and vascular resistance among hypoxic rats and controls.CONCLUSION: Capillary proliferation does not occur in skeletal muscle of rat exposed to hypoxia merely. However, skeletal muscle fiber atrophy caused by hypoxia induces relative increase of CD.