Cardiac hypertrophy and its regression in rat: Comparison of morphological changes in response to aortic constriction, iron deficiency anaemia and isoprenaline

Morphological changes were studied and compared in three models of cardiac hypertrophy and its regression in the rat—subdiaphragmatic aortic constriction, chronic isoprenaline treatment and iron deficiency anaemia. Mitochondrial volume density remained normal with aortic constriction but increased w...

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Published inJournal of molecular and cellular cardiology Vol. 14; no. 9; pp. 501 - 512
Main Authors Sung, R., Stephens, M., Blayney, L., Henderson, A.
Format Journal Article
LanguageEnglish
Published England Elsevier Ltd 01.09.1982
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ISSN0022-2828
1095-8584
DOI10.1016/0022-2828(82)90211-5

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Summary:Morphological changes were studied and compared in three models of cardiac hypertrophy and its regression in the rat—subdiaphragmatic aortic constriction, chronic isoprenaline treatment and iron deficiency anaemia. Mitochondrial volume density remained normal with aortic constriction but increased with isoprelanine-induced hypertrophy and with iron deficiency anaemia; the surface to volume ratio was increased (implying smaller mitochondria) with aortic constriction and with isoprenaline treatment, but remained normal in iron deficiency anaemia. Regression of all the morphological changes was complete ten days after discontinuing the hypertrophic stimulus in all models. Regression of heart/body weight ratios was complete after 14 days in the aortic constriction and isoprenaline models, but remained incomplete at 80 days in the iron deficiency model. Low heart/body weight ratios at 15 months were observed following an earlier period of mechanically induced hypertrophy, consistent with a premature ageing effect. The results suggest that factors regulating the maintenance myofibrillar volume density are common to different models of hypertrophy but mitochondrial size and volume density are subject to additional controlling influences.
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ISSN:0022-2828
1095-8584
DOI:10.1016/0022-2828(82)90211-5