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主动脉狭窄大鼠心房肌细胞中的DNA合成

DNA synthesis in atrial myocytes of rats with aortic stenosis.

作者信息

Rumyantsev P P

出版信息

Adv Myocardiol. 1983;4:147-62. doi: 10.1007/978-1-4757-4441-5_12.

Abstract

Indices of labeled myonuclei have been determined in hypertrophying hearts of adult Wistar rats by autoradiography after single-pulse or repeated [3H]thymidine administration. After single [3H]thymidine injections, only 1.36 +/- 0.66 and 1.32 +/- 0.87% labeled myonuclei were observed in the left and right atria, respectively. In the experiments with multiple [3H]thymidine administration, the first injection of this precursor was given on the seventh day after aortic constriction; thereafter, 30 or 42 injections of [3H]thymidine were given at 12-hr intervals up to the fourth postoperation week. Following 30 repeated [3H]thymidine injections, 29.75 +/- 4.65 and 16.78 +/- 3.33% labeled myonuclei were visible in left and right atrial muscle cells, respectively. The cumulative labeling index for left atrium myocytes clearly correlates (r = 0.65-0.73) with an increase in the weight of the heart. Increase in heart weight to more than 160% of controls corresponds to [3H]thymidine labeling of 38.06 +/- +/- and 21.67 +/- 4.16% in left and right atrial myocytes, respectively, whereas in hearts weighing less than 140% of controls, [3H]thymidine labels only 8.20 +/- 1.93% in the left atrium and 3.94 +/- 1.57% in the right one. In the ventricles, cumulative indices of myonuclear labeling do not exceed 0.217 +/- 0.11% even in hearts weighing nearly 180% of controls. Cumulative frequencies of labeling for AV system myocytes are almost ten times higher (1.97 +/- 0.38). These results, together with our data concerning mycocardial infarction (27-29,31), make it necessary to reconsider the role of cardiomyocyte hyperplasia in different experimental and pathological conditions, paying special attention to the proliferative behavior of the atrial muscle cells. DNA synthesis in atrial myocytes seems to be stimulated by heart hyperfunction.

摘要

在成年Wistar大鼠的心脏肥大模型中,通过单次脉冲或重复注射[³H]胸腺嘧啶核苷后进行放射自显影,测定了标记肌核的指标。单次注射[³H]胸腺嘧啶核苷后,在左心房和右心房中分别仅观察到1.36±0.66%和1.32±0.87%的标记肌核。在多次注射[³H]胸腺嘧啶核苷的实验中,在主动脉缩窄后第7天首次注射该前体;此后,每隔12小时注射30次或42次[³H]胸腺嘧啶核苷,直至术后第四周。在30次重复注射[³H]胸腺嘧啶核苷后,在左心房和右心房肌细胞中分别可见29.75±4.65%和16.78±3.33%的标记肌核。左心房心肌细胞的累积标记指数与心脏重量的增加明显相关(r = 0.65 - 0.73)。心脏重量增加至超过对照组的160%时,左心房和右心房心肌细胞中[³H]胸腺嘧啶核苷标记分别为38.06±??和21.67±4.16%,而在重量小于对照组140%的心脏中,[³H]胸腺嘧啶核苷在左心房的标记仅为8.20±1.93%,在右心房为3.94±1.57%。在心室中,即使在心脏重量接近对照组180%的情况下,肌核标记的累积指标也不超过0.217±0.11%。房室系统心肌细胞的累积标记频率几乎高十倍(1.97±0.38)。这些结果,连同我们关于心肌梗死的数据(27 - 29,31),使得有必要重新考虑心肌细胞增生在不同实验和病理条件下的作用,特别关注心房肌细胞的增殖行为。心房肌细胞中的DNA合成似乎受到心脏功能亢进的刺激。 (注:原文中“38.06 +/- +/-”表述有误,翻译时保留原文错误)

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