Title: Norepinephrine and cardiac hypertrophy in iron deficiency anemia
Abstract: Myocardial hypertrophy is a morphological adaptive response to chronic work overload imposed on the heart. It has been categorized into two distinct basic types: concentric hypertrophy, occurring in response to a sustained pressure overload in which wall thickness increases without chamber enlargement, and eccentric hypertrophy, in response to a chronic volume overload in which chamber volume enlarges without a relative increase in its wall thickness. It should be emphasized, in this context, that these adjectives are somewhat confusing, since the hypertrophy observed is not eccentric in the fashion often seen in the left ventricle of patients with hypertrophic cardiomyopathy. In fact, the hypertrophy is concentric in both instances, but is associated with an increase in chamber volume when described as eccentric, yet occurring with a maintained volume when said to be concentric. In rats made anemic by iron deficiency, the volume overloaded heart achieves an adaptive increase in mass characterized as hypertrophy occurring in the setting of dilated ventricle. This so-called eccentric hypertrophy depends on catecholamines as possible signals for myocardial growth, and progresses with preserved ultrastructure and contractile performance of the cardiac muscle. A gradually imposed volume overload results in a harmonious growth of the heart (it retains a relative normal shape, becoming a magnified normal heart), probably mediated by release of catecholamines into the myocardium. This process resembles the normal cardiac growth in response to the obligatory volume load imposed by an increasing cardiac output (greater metabolic demands) and blood volume. On the other hand, in the rat heart overloaded in terms of pressure by constriction of the abdominal aorta, an adaptive augmentation in mass is characterized as concentric hypertrophy (mural hypertrophy without any change in volume), in which catecholamines may not play a dominant role. This progresses with altered ultrastructure and contractile function of the myocardium. The character, degree, and duration of the work induced by an overload, itself produced by volume and pressure, in isolation or combined, therefore plays a critical role in determining the course of the process of hypertrophy. We argue that it is a plausible hypothesis that the cardiac hypertrophy induced by overload as a consequence of a change in volume, in contrast to hypertrophy induced by overload as a consequence of pressure, are distinctly different biological phenomena mediated through different mechanisms.
Publication Year: 1983
Publication Date: 1983-05-01
Language: en
Type: letter
Indexed In: ['crossref', 'pubmed']
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Cited By Count: 1
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