Structural Alterations in the Hypertrophied and Failing Myocardium

Bishop, Sanford P.

doi:10.1007/978-1-4613-3825-3_18

Cited by 5 publications

(4 citation statements)

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“…40 When analyzed through its entire life span, the ventricular consequences of long-term hypertension in the SHR can be better appreciated. 52 The heart is an organ that is in a steady state regarding its energy producing and consuming cells and organelles. 53 Therefore, any impairment in the flow of energy producing substrates and/or oxygen is compounded by a corresponding increase in metabolic byproducts that may profoundly influence contractility and function.…”

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Morphometric analysis of cardiac hypertrophy during development, maturation, and senescence in spontaneously hypertensive rats.

Engelmann¹,

Vitullo²,

Gerrity³

1987

Circulation Research

105

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Hypertrophy of the mammalian heart, regardless of the initiating event, results in architectural remodeling of ventricular components that maintain structural and functional characteristics of this organ. Ventricular components that vary their morphology and morphometry in a hypertrophic state are the muscle cells, connective tissue elements, vasculature, or a combination of some or all of the above. Morphologic quantification of the progressive tissue changes occurring throughout the natural life span of the spontaneously hypertensive and normotensive Wistar-Kyoto rats has not been thoroughly documented. Using perfused-fixed tissue from both strains at 1, 6, 12, 18, and 24 months of age, we have determined the morphometric changes that occurred in the subepicardial and midwall regions of the left ventricle. Myocyte cell size, wall thickness, and arterial blood pressure were elevated in 1-month-old spontaneously hypertensive rats, reached significance by 6 months, and remained significantly greater throughout the 24 months examined. Tissue morphometry demonstrated significant tissue component volumetric differences at 6 months in the spontaneously hypertensive rat. Age-related morphometric tissue changes occurred in both strains yet were exacerbated (percent volume of myocytes) or diminished (percent volume interstitial space) in the mature and aging spontaneously hypertensive rat. Capillary density of SHR left ventricle showed a drastic decline so that 6-month-old SHR had the same density as a senescent Wistar-Kyoto. Tissue morphometry and capillary density data strongly support the hypothesis that tissue oxygenation is diminished in the spontaneously hypertensive rat, and as a result, tissue necrosis and myocyte cell death occur. H ypertrophy of the heart, regardless of the initiating event, is the structural consequence of one or more factors. These factors include increases in the number and/or size of myocytes, the amount of connective tissue elements or vasculature, or a combination of all or some of the above. The spontaneously hypertensive rat (SHR) represents an oft-analyzed model of human essential hypertension 1 wherein the preferential association between hypertension and cardiac hypertrophy can be manipulated and often disassociated.23 While morphometric analyses of hypertension-stimulated cardiac hypertrophy are present in the literature, 4 " 12 the morphologic progression of hypertrophy throughout the natural life span of the SHR has not been thoroughly documented. Of particular interest during this morphologic progression are myocardial vasculature changes that occur throughout the life span of normotensive and spontaneously hypertensive rats. Wearn and Roberts and Wearn first showed that the increase in myocardial mass associat- Supported by National Heart. Lung, and Blood Institute grant HL-25940.Address for correspondence and reprints: Gary L. Engelmann, PhD, Research Institute, Department of Heart and Hypertension (FF4), The Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44106...

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confidence: 99%

Morphometric analysis of cardiac hypertrophy during development, maturation, and senescence in spontaneously hypertensive rats.

Engelmann¹,

Vitullo²,

Gerrity³

1987

Circulation Research

105

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“…Expansion of Z-line material is present in a variety of animals with experimentally induced or naturally , occurring hypertrophy and failure (10,12,37,42), as well as in hypertrophied human myocardium (23,25). The expanded Z-lines consist ofelectron-dense material which may be diffuse in nature or, more often, has a characteristic parallel arrangement of fibrils with an approximately 200 A spacing (Fig.…”

Section: Ultrastructural Alterations Ofmyocytes In Cardiac Hypertrophymentioning

confidence: 99%

The Myocardial Cell: Normal Growth, Cardiac Hypertrophy and Response to Injury

Bishop

1990

Toxicol Pathol

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Development and growth of cardiac muscle tissue is controlled by a variety of intrinsic and extrinsic factors. Fetal growth is by hyperplasia, is strongly governed by inherent factors and is only slightly modified by external environmental factors. The number of cell divisions is species-dependent and normally stops shortl~after birth. Developing blood volume and pressure dictate the hypertrophic stage of normal growth, and this may be further modified by abnormal hemodynamic and humoral factors. Connective tissue, neural and vascular components of the myocardium mature along with the myocyte, and alterations in these structures profoundly affect myocyte function. Hypertrophy beyond normal growth is the response of the myocyte by increased protein synthesis to various stimuli including hemodynamic, humoral and ischemic factors. Injury to normal and hypertrophied myocardium may vary due to structural and metabolic adaptations of hypertrophied tissue, such as connective tissue proliferation, vascular supply alterations and glycolytic metabolic potential. Ischemic effects influence not only cell necrosis, but also hypertrophy and congestive myocardial failure.

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“…During the neonatal growth period of the rat, ventricular myocytes cease to divide and become binuclear. All early increases in heart size are due to an approximate 30-to 40-fold increase (hypertrophy) in individual myocyte volume (Bishop, 1984;Zak, 1984). Because the ventricle is composed of several different types of cells, enlargement of the ventricular myocyte occurs, along with concomitant increases in the number of non-myocyte cells (Zak et al, 1979;Zak, 1984).…”

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“…Physiological hypertrophy of the myocyte is a normal component of heart maturation, during which both functional and structural development of the myocardium occurs (Bishop, 1984). During the neonatal growth period of the rat, ventricular myocytes cease to divide and become binuclear.…”

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Age-related changes in ploidy levels and biochemical parameters in cardiac myocytes isolated from spontaneously hypertensive rats.

Engelmann¹,

Vitullo²,

Gerrity³

1986

Circulation Research

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Postnatal growth of the mammalian ventricular myocyte is characterized by a brief period of hyperplasia followed by an extensive period of physiological hypertrophy. Using myocytes isolated from both Wistar-Kyoto and spontaneously hypertensive rats from fetus to 10 months old, we analyzed morphological, biochemical, and ploidy changes. Fetal myocytes from both spontaneously hypertensive and Wistar-Kyoto rats were mononuclear, diploid cells. By 4 weeks, adult binucleation levels (84% binuclear) were found, and myocytes pooled from both ventricles demonstrated nuclear ploidy shifts to tetraploid levels. However, analysis of myocytes isolated from left ventricle, right ventricle, and septum showed that nuclear polyploidation was confined to the right ventricle and septum, with few polyploid nuclei detected in the left ventricle. This pattern remained relatively constant through 10 months of age, although spontaneously hypertensive myocytes showed significantly more polyploidation than Wistar-Kyoto in all regions. Biochemical analysis of isolated myocytes substantiated the nuclear ploidy changes and demonstrated elevated protein and ribonucleic acid content in left ventricular myocytes without extensive polyploidation. Since cardiac hypertrophy, both physiological and pathological, is associated primarily with the left ventricle and occurs in the absence of significant ploidy changes, these findings suggest that a unique pattern of gene regulation may be ongoing in the left ventricle myocytes that is not present in the septum and right ventricle. These variations may be essential for cellular hypertrophy under normal and pathological conditions.

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Structural Alterations in the Hypertrophied and Failing Myocardium

Cited by 5 publications

References 85 publications

Morphometric analysis of cardiac hypertrophy during development, maturation, and senescence in spontaneously hypertensive rats.

Morphometric analysis of cardiac hypertrophy during development, maturation, and senescence in spontaneously hypertensive rats.

The Myocardial Cell: Normal Growth, Cardiac Hypertrophy and Response to Injury

Age-related changes in ploidy levels and biochemical parameters in cardiac myocytes isolated from spontaneously hypertensive rats.

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