Rumiantsev P P, Koro Antich R M, Nilova V K
Tsitologiia. 1987 Jan;29(1):35-46.
As a result of 30 times repeated injections of 3H-thymidine (3HTdr) to neonate rats, beginning from days 13 or 21 post partum, ca. 20 and 10% of myonuclei in the left and right atria were labeled, respectively, while in both ventricles cumulative labeling of myocytes was nearly ten times lower. In rats of the same age with experimental infarction of the left ventricular myocardium the number of myonuclei labeled after 30-fold 3HTdr injections increased in atria up to 40-50%, in perinecrotic myofibers of the left ventricles up to 8-11%, and in myofibers of the left and right ventricle located far from the necrotic foci up to 3-4 and 2-3%, respectively. In some of rats subendocardial and/or subepicardial layers of the surviving left ventricular myocardium contained up to 15-35% of labeled myonuclei. Thus, in neonatal rats the extent of DNA synthesis reactivation in the nuclei of cardiomyocytes, the majority of which have recently completed normal ontogenetic proliferation, is, on the whole, of the same order as found in similar experiments on adult rats (Rumiantsev, Kassem, 1976; Oberpriller et al., 1984). However, still immature ventricular myocytes of neonatal rats resume mitotic cycle easier than those of adult animals which is evidenced not only by higher numbers of 3HTdr labeled myonuclei in subepicardial and subendocardial ventricular myocardia of some rats, but even more by reactivation of DNA synthesis in a limited fraction (2-3%) of the whole population of non-perinecrotic myocytes in both ventricles. Besides, reactive proliferation of cardiomyocytes in the atria of neonate rats, unlike in adults, starts on day 3 rather than on day 5 after infarction is induced. In the atria of neonatal rats polyploidization of myonuclei at later postinfarction stages is less pronounced than in adult rats which may be accounted for by formation of individual daughter nuclei during acytokinetic mitoses or, more seldom, by completion of cytotomy.
从产后第13天或21天开始，对新生大鼠重复注射30次3H-胸腺嘧啶核苷（3HTdr），结果显示，左心房和右心房中分别约有20%和10%的肌细胞核被标记，而在两个心室中，心肌细胞的累积标记率几乎低10倍。在同龄的左心室心肌实验性梗死大鼠中，注射30次3HTdr后，心房中被标记的肌细胞核数量增加到40%-50%，左心室坏死周围肌纤维中增加到8%-11%，远离坏死灶的左、右心室肌纤维中分别增加到3%-4%和2%-3%。在一些大鼠中，存活的左心室心肌的心内膜下和/或心外膜下层含有高达15%-35%的标记肌细胞核。因此，在新生大鼠中，心肌细胞核中DNA合成再激活的程度，总体上与在成年大鼠的类似实验中发现的程度相同（鲁缅采夫、卡塞姆，1976年；奥伯普里尔等人，1984年）。然而，新生大鼠仍未成熟的心室肌细胞比成年动物的心室肌细胞更容易恢复有丝分裂周期，这不仅表现为一些大鼠心外膜下和心内膜下心室心肌中3HTdr标记的肌细胞核数量更多，而且更表现为两个心室中非坏死心肌细胞总数的有限部分（2%-3%）中DNA合成的再激活。此外，与成年大鼠不同，新生大鼠心房中的心肌细胞反应性增殖在梗死诱导后第3天而非第5天开始。在新生大鼠的心房中，梗死后期肌细胞核的多倍体化不如成年大鼠明显，这可能是由于无胞质有丝分裂过程中单个子核的形成，或者更少见的是由于胞质分裂的完成。
