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在大鼠急性和慢性心肌梗死后,心室负荷与成年心肌细胞中的DNA合成相关联。

Ventricular loading is coupled with DNA synthesis in adult cardiac myocytes after acute and chronic myocardial infarction in rats.

作者信息

Capasso J M, Bruno S, Cheng W, Li P, Rodgers R, Darzynkiewicz Z, Anversa P

机构信息

Department of Medicine, New York Medical College, Valhalla 10595.

出版信息

Circ Res. 1992 Dec;71(6):1379-89. doi: 10.1161/01.res.71.6.1379.

DOI:10.1161/01.res.71.6.1379
PMID:1423934
Abstract

To determine whether the overload associated with myocardial infarction and ventricular failure in rats is coupled with activation of DNA synthesis in the remaining left and right ventricular myocytes, flow cytometric analysis was performed on myocyte nuclei prepared from both ventricles 7 and 30 days after coronary occlusion. In addition, oral captopril was administered in separate groups of control and experimental rats to establish whether a relation existed between attenuation of ventricular loading and magnitude of DNA synthesis in myocytes. Results demonstrated that left ventricular failure and right ventricular dysfunction at 7 days after infarction were biventricularly associated with marked increases in the number of myocyte nuclei in the G2M phase of the cell cycle. In contrast, the fraction of nuclei in the G0+G1 phase decreased. In comparison with the earlier time point, the 30-day interval was characterized by a significant magnitude of cardiac hypertrophy, a moderate amelioration of ventricular pump function, and a decrease in the percentage of myocyte nuclei in the G2M phase in both ventricles. However, 30 days after infarction, the number of right ventricular myocyte nuclei in the S and G2M phases remained elevated with respect to control animals. Captopril therapy reduced the extent of ventricular loading and the population of myocyte nuclei in the cell cycle at 7 days. In conclusion, DNA synthesis in myocyte nuclei may represent an important adaptive component of the myocardial response to infarction.

摘要

为了确定与大鼠心肌梗死和心室衰竭相关的负荷增加是否与左、右心室剩余心肌细胞中DNA合成的激活有关,在冠状动脉闭塞后7天和30天,对从两个心室制备的心肌细胞核进行了流式细胞术分析。此外,对单独的对照组和实验组大鼠给予口服卡托普利,以确定心室负荷减轻与心肌细胞中DNA合成量之间是否存在关联。结果表明,梗死7天后左心室衰竭和右心室功能障碍与细胞周期G2M期心肌细胞核数量显著增加呈双心室相关。相比之下,G0+G1期细胞核的比例下降。与早期时间点相比,30天间隔的特征是心脏肥大程度显著、心室泵功能适度改善以及两个心室中G2M期心肌细胞核百分比下降。然而,梗死30天后,与对照动物相比,右心室S期和G2M期心肌细胞核数量仍然升高。卡托普利治疗在7天时降低了心室负荷程度和细胞周期中心肌细胞核的数量。总之,心肌细胞核中的DNA合成可能代表心肌对梗死反应的一个重要适应性组成部分。

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