DNA content, ploidy level and number of nuclei in the human heart after myocardial infarction
DNA content, ploidy level and number of nuclei in the human heart after myocardial infarction
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DOI：
10.1016/s0008-6363(97)00140-5
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发表时间：
1997-10-01
影响因子：
10.8
通讯作者：
Adler, CP
中科院分区：
文献类型：
--
作者：
Herget, GW;Neuburger, M;Adler, CP
目的：心肌功能活动延长引起的心肌肥大与细胞大小的增加和心肌细胞核的多倍体化有关。心肌梗塞的特征是心肌细胞的丧失。负荷增加，因此存活心肌肥厚生长是可以预料的。本研究的目的是研究心肌细胞在梗死后的反应。方法：对心肌细胞和结缔组织细胞核进行生化和细胞光度分析，确定心肌梗死后的人心脏是否伴随倍性水平、DNA含量和细胞核数量的增加。从尸检材料中获得的心脏共15颗，其中心肌梗死后8颗。用间接计算法测定了核数。结果：心肌梗死后4c核减少，2c核无明显差异。心肌梗死后DNA倍体水平（bbb80c）及非整倍体心肌细胞核比例升高。心肌梗死后心肌DNA浓度和总DNA含量均升高。心肌梗死后结缔组织核/肌细胞核数比、核总数、肌细胞核数、结缔组织核数均增加。结论：心肌细胞的多倍体化和细胞核增生可能是心肌对缺血损伤的适应性反应。(C) 1997爱思唯尔科学有限公司
Objective: Cardiac hypertrophy due to a prolonged functional activity is associated with an increase of cell size and polyploidization of the myocyte nuclei. Myocardial infarction is characterized by loss of myocytes. Increased load and as a consequence hypertrophic growth of the surviving myocardium has to be expected. The aim of this study was to investigate the response of cardiomyocytes after infarction. Method: Biochemical and cytophotometric analysis was performed on myocyte and connective tissue nuclei to determine whether the human heart after myocardial infarction is accompanied by an increase in the ploidy level, DNA content and in the number of nuclei. A total of 15 hearts obtained from autopsy material was studied, among them 8 after myocardial infarction. The number of nuclei was measured by indirect computation. Results: We found a decrease of 4c and no significant difference of 2c nuclei in infarcted hearts. DNA ploidy level (> 8c) as well as the proportion of aneuploid myocyte nuclei were increased in infarcted hearts. DNA concentration and total DNA content were increased in the hearts after myocardial infarction. Numerical ratio of connective tissue nuclei/myocyte nuclei, total number of nuclei, number of myocyte nuclei and number of connective tissue nuclei were increased in infarcted hearts. Conclusion: Polyploidization and nuclear hyperplasia of myocytes may represent an adaptive response of the myocardium to an ischemic injury. (C) 1997 Elsevier Science B.V.