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Research Article Free access | 10.1172/JCI113278

Hyperplasia of myocyte nuclei in long-term cardiac hypertrophy in rats.

G Olivetti, R Ricci, and P Anversa

Department of Pathology, University of Parma, Italy.

Find articles by Olivetti, G. in: JCI | PubMed | Google Scholar

Department of Pathology, University of Parma, Italy.

Find articles by Ricci, R. in: JCI | PubMed | Google Scholar

Department of Pathology, University of Parma, Italy.

Find articles by Anversa, P. in: JCI | PubMed | Google Scholar

Published December 1, 1987 - More info

Published in Volume 80, Issue 6 on December 1, 1987
J Clin Invest. 1987;80(6):1818–1821. https://doi.org/10.1172/JCI113278.
© 1987 The American Society for Clinical Investigation
Published December 1, 1987 - Version history
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Abstract

In contrast to observations made in the human heart, hyperplasia of myocyte nuclei has never been demonstrated in experimental cardiac hypertrophy. To test the hypothesis that the duration of the mechanical load more than the magnitude of ventricular hypertrophy may be the inciting stimulus for myocyte nuclei hyperplasia, constriction of the pulmonary artery was produced in rats and the hearts were examined 6 mo later. A 76% increase in right ventricular weight was measured. This hypertrophic response was accompanied by a 41% increase in the total number of myocyte nuclei in the ventricle. Furthermore, average myocyte cell volume per nucleus increased by 28%. No changes in weight, myocyte size, and nuclear number were observed in the left ventricle. In conclusion, myocyte nuclear hyperplasia and cellular hypertrophy both participate to the adaptive response of the right ventricular myocardium in long-standing pressure overload cardiac hypertrophy.

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