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  • Title: Myocardial DNA content, ploidy level and cell number in geriatric hearts: post-mortem examinations of human myocardium in old age.
    Author: Adler CP, Friedburg H.
    Journal: J Mol Cell Cardiol; 1986 Jan; 18(1):39-53. PubMed ID: 3950970.
    Abstract:
    A reduced adaptation rate of the myocardium must, in many cases, be made responsible for heart insufficiency of old patients. The present investigations are aimed towards the question whether heart in old age is accompanied by a loss of myocardial cells and whether a polyploidisation of heart muscle cells takes place thus indicating an adaptive process. A total of 40 human hearts obtained from autopsy material were studied, among them 30 geriatric hearts. Following preparation of the hearts, the myocardium was weighed and the total amount of DNA was determined biochemically. By means of Feulgen cytophotometry the ploidy levels of the heart muscle nuclei were detected. We have used a special method for estimating the total number of heart muscle cells and connective tissue cells in the individual hearts. It could be shown that the total amount of DNA in the myocardium is correlated with the myocardial weight and not with the age of the individual. Instead, DNA synthesis occurs in the heart muscle cells of all age groups depending on the functional activity of the heart. The degree of polyploidisation is closely correlated with myocardial hypertrophy without any influence of age. In hypertrophic hearts the number of connective tissue cells increases from normally 4 to 5 X 10(9) to 12 X 10(9) (in hearts weighing more than 700 g); in hearts with interstitial fibrosis these values are even higher. In normal hearts 1.8 to 2.1 X 10(9) heart muscle cells can be estimated; in hearts weighing more than 500 g numerical hyperplasia of the heart muscle cells is produced, reaching a maximum number of 4.8 X 10(9) muscle cells in excessively hypertrophied hearts weighing more than 800 g. No correlation between age and myocardial cell number (i.e. heart muscle cells or connective tissue cells) could be observed. This means that no agespecific changes occur in the myocardium with regard to the DNA content and cell number. The structural changes found in the hearts of old individuals are produced by extracardial influences (i.e. arteriosclerosis, hypertension, etc.) leading to myocardial hypertrophy. Polyploidisation and augmentation of heart muscle cells in cardiac hypertrophy or decrease in the number of heart muscle cells in heart atrophy may occur at any time of life and are not age-specific.
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