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  • Title: Cumulative indices of DNA synthesizing myocytes in different compartments of the working myocardium and conductive system of the rat's heart muscle following extensive left ventricle infarction.
    Author: Rumyantsev PP, Kassem AM.
    Journal: Virchows Arch B Cell Pathol; 1976 May 26; 20(4):329-42. PubMed ID: 820062.
    Abstract:
    Ten successive 3H-thymidine injections at 12 h intervals (which is a little shorter than the adult heart myocyte S phase) were performed for labeling of the majority of cardiac myocytes synthesizing DNA at any moment of such a 5 days experiment. In the hearts of control unoperated rats ten-fold repeated 3H-thymidine administration results in labeling of 2-3% myocyte nuclei in both atria, ca. 1% of the specialized muscle cell nuclei in the atrioventricular conductive system, only occasional muscle cells being labeled in the working ventricular myocardium. When ten successive 3H-thymidine injections were made between the 5th and 10th days following extended left ventricle infarction, the percentage of labeled myocytes in left and right atria reaches, respectively, 51.4 +/- 4.4% and 34.7 +/- 3.6%. In the left ventricle labeled muscle nuclei are accumulated predominantly (9.3 +/- 2.1%) within the thin subepicardial layer of the surviving myofibers, while myofibers located in other perinecrotic areas contained only 1.3 +/- 0.5% labeled muscle nuclei. The number of these nuclei in the atrioventricular system remains at the level observed in control hearts (up to 2%), approaching closely the zero level in the working myocardium of both the ventricles and interventricular septum, located at the considerable distance from the infarcted region. When similar experiments with ten-fold repeated 3H-thymidine injections were performed between 15th and 20th post-infarction days the number of labeled myocyte nuclei was found to be reduced 4-6 times in atria, being changed rather a little in the perinecrotic ventricular myocardium and in the specialized myocardium of the atrioventricular system. Some possible reasons of the observed differences in the proliferative behaviour of cardiac myocytes in terms of their topology and/or specialization are discussed.
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