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作 者:李娜娜[1] 王庆志[1] 周立[1] 张红旗[2]
机构地区:[1]新乡医学院人体解剖学教研室,河南新乡453003 [2]复旦大学上海医学院解剖与组织胚胎学系,上海200032
出 处:《中国临床解剖学杂志》2011年第4期433-435,共3页Chinese Journal of Clinical Anatomy
基 金:河南省杰出青年科学基金(NO.2005HANCET-15)
摘 要:目的利用光镜和透射电镜观察动脉粥样硬化兔窦房结组织,特别是对起搏细胞和过渡细胞结构的影响。方法兔20只,分为对照组和高脂组两组。高脂组饲高脂饮食,对照组饲普通饮食。光镜和透射电镜观察窦房结组织及其细胞、间质的结构变化。结果高脂组心肌组织中有粥样硬化斑块的形成,间质内有大量脂质沉积、浸润。透射电镜下,高脂组起搏细胞和过渡细胞内有大量脂滴,且成纤维细胞、心肌细胞、间质内及髓样结构周围均有脂滴的存在。结论动脉粥样硬化导致窦房结组织脂肪沉积,结内各种细胞脂质化,可能是影响窦房结起搏冲动的产生、发放和传递,导致其电生理活动异常的形态学基础。Objective To explore the effects of atherosclerosis on the morphological changes of rat sinoatrial node (SAN), especially the features of pacemaker cells and transitional cells under light microscopy and transmission electron microscopy. Methods 20 New Zealand white rabbits were randomly allocated to control group and hyperlipidemia group, with 10 animals in each group. The control animals were fed with routine forage, but animals of the hyperlipidemia group was fed with high lipid forage about 3 months. Histologic changes of SAN were studied through serial sections and transmission electron. Results Atherosclerotic plaques and extensive lipid infiltration appeared in myocardium tissue and cell matrix of hyperlipidemia animals separately. Transmission electron microscope revealed that a large number of lipid droplets aggregated in pacemaker cells, transitional cells, interstitial cells and interstitial matrix. Conclusions Atherosclerosis causes fat deposition in SAN. Lipid infiltration in SAN may damage impulse generation, transmission and distribution and thereby provide morphological basis for spontaneous activity.
关 键 词:动脉粥样硬化 起搏细胞 过渡细胞 脂质 窦房结 兔
分 类 号:R322.1[医药卫生—人体解剖和组织胚胎学]
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