摘要
目的:观察实验性高脂血症及慢性间歇低氧对大鼠心肌超微结构的影响,探讨其可能的机制。方法:72只雄性Wistar大鼠随机均分为3组,空白对照组普通鼠料喂养,高脂组高脂饲料喂养,高脂+间歇低氧组高脂饲料喂养,同时给予7h/d间歇低氧处理。观察3组大鼠3、6和9周末心肌结构改变。结果:空白对照组大鼠心肌结构未见异常,高脂组心肌细胞具有多种超微病理改变,高脂+间歇低氧组损伤更为明显。损伤主要表现为心肌细胞核染色质局灶性溶解,肌丝溶解,膜结构破坏,心肌细胞间质中微血管内皮细胞水肿、变性,管腔内可见活化状态血小板。结论:高脂+慢性间歇低氧复合条件下对心肌超微结构损伤较高脂组更为明显,且随时间推移损伤逐渐加重。
Objective：To observe the effect of experimental hyperlipidemia and chronic intermittent hypoxia on myocardial ultrastructure in rats,and to investigate the mechanism of it.Methods：Seventy -two male Wistar rats were randomly assigned into 3 groups which were fed to normal diet（control group）,cholesterol-high-fat diet（high-fat group） and high-fat diet plus intermittent hypoxia treatment for 7 hours every day（high-fat/hypoxia group）.Then the ultrastructures of the chest aorta on the time point of 3,6 and 9 weeks were observed by transmission electron microscope.Results：There were no pathological changes in control group.However multiple changes in myocardium were found in high-fat group,and much more serious injuries in the high-fat/hypoxia group.The pathological injury was slight in 3 weeks,and became serious in 6 weeks and more serious in 9 weeks,including focal lysis of chromatin in the nucleus,lysis of myofilament,disorganization of membrane structure in myocardial cells.The endothelial cells of capillary vessel in intercellular substance showed swell and denaturation,and platelet showed activated state on the lumen surface.Conclusion：Combined hyperlipidemia with chronic intermittent hypoxia made more injury in myocardial ultrastructure than that of hy perlipidemia alone.The injury became serious on time-dependent effect.
出处
《天津医药》
CAS
北大核心
2008年第11期888-890,I0002,共4页
Tianjin Medical Journal
基金
中央保健委员会保健专项资金资助项目(津A002)
