摘要
目的：研究心衰时心肌细胞线粒体的立体构筑形态学改变，为心衰机理提供科学依据。方法：用Ｗｉｓｔａｒ大鼠制作后负荷心衰模型；分离心肌细胞；用Ｔｒｉｔｏｎｘ１００去心肌细胞膜和游离蛋白质；制备游离心肌细胞整装骨架，干燥，喷金，日立Ｓ—４５０扫描电镜下观察。结果：心衰时心肌细胞发生线粒体肿胀，固定装置破坏、缺失与移位等形态学改变。结论：线粒体固定装置破坏；线粒体肿胀肥大以及线粒体移位与缺失是心力衰竭时能量供应障碍、心功能低下的物质基础。
Objective: Our aims
were to study the morphological changes of threedimentional architecture of mitochondria in
afterload heartfailure and to provide the scientific evidence for heart failure mechanism.
Methods: We used Wistar rats to set up the afterload heart failure model.Then we isolated the
cardiac myocytes of the models with collagenase and got rid of the myocyte membrane and free
myocyte protein with Tritonx 100. The whole cytoskeleton of the isolated cardic myocytes were
casted and observed by S450 scanning electron microscopy. Results:5BZThe mitochondria
was swollen and the morphological changes of its fixed apparatus such as injury,absence and
dislocation were observed for rats with heart failure. Conclusion: The substance basis of heart
dysfunction and energy supply disorder in heart failure included the damage of fixed apparatus
of mitochondria,enlargement and atrophy of mitochondria and the dislocation and deficiency of
mitochondria.
出处
《中国医科大学学报》
CAS
CSCD
北大核心
1999年第3期174-175,178,共3页
Journal of China Medical University
