In addition, we performed histopathologic evaluation of these slides, which led to the elimination of four hearts. Scale bar: 50 μm () noncardiomyocyte nuclei on three random myocardial sections from different sites of the same LV shows no significant differences in the nuclear density in different compartments of the same LV. The resulting yield of cardiomyocytes was 91.3 ± 3% [weight%, determined by (original weight – residual)/original weight].Thus, evaluation of the selected hearts showed that they are a representative sample () noncardiomyocyte nuclei on three random myocardial sections from different sites of the same LV shows no significant differences in the nuclear density in different compartments of the same LV. The percentage of cardiomyocytes with desmosome-containing ends was 92.4 ± 0.4% (Fig.Our current understanding of human myocardial growth is limited by an overall lack of reliable data about the underlying cellular mechanisms (reviewed in refs. Cardiomyocyte nuclei have been quantified in human fetuses using hematoxylin-eosin staining (13–15).Radiocarbon birth dating has shown that a small portion of cardiomyocytes is replaced in humans older than 20 y (16), but this technique is unreliable for the analysis of recent samples from individuals younger than 20 y of age (17).
For example, in mice, developmental cardiomyocyte proliferation continues for up to day 7 after birth, which coincides with the loss of regenerative capacity (11, 12).
The human heart is believed to grow by enlargement but not proliferation of cardiomyocytes (heart muscle cells) during postnatal development.
However, recent studies have shown that cardiomyocyte proliferation is a mechanism of cardiac growth and regeneration in animals.
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