The growth of the muscular and collagenous parts of the rat heart in various forms of cardiomegaly

Bartosova, D; Chvapil, Miloš; Korecký, B.; Poupa, O; Rakusan, K; Turek, Z.; Vízek, M

doi:10.1113/jphysiol.1969.sp008693

Cited by 174 publications

(79 citation statements)

References 22 publications

(13 reference statements)

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“…In contrast to aortic-coarctation or DOC/salt-induced cardiac hypertrophy (6,(34)(35)(36), the hypertrophy induced by triiodothyronine is known to be biventricular with an absence of obvious myocyte loss, focal necrosis, fibrosis, or other major histological abnormalities (23,37). Triiodothyronine effects on the heart are a result of complex interactions between peripheral and direct effects.…”

Section: Resultsmentioning

confidence: 99%

Fibronectin expression in the normal and hypertrophic rat heart.

Mamuya¹,

Brecher²

1992

J. Clin. Invest.

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We examined changes in the expression of fibronectin during the induction of cardiac hypertrophy by L-triiodothyronine administration and by mineralocorticoid-and salt-induced experimental hypertension. By use of Northern and Western blotting procedures, fibronectin was localized mainly in the atria of normal rat hearts. Atria contained 10-and 5-fold higher relative concentrations of fibronectin mRNA and protein, respectively, compared with ventricles. During the progression of cardiac hypertrophy induced by L-triiodothyronine over a 10-d period, there was a progressive increase in fibronectin mRNA for the first 6 d followed by a return to control levels. The major change could be accounted for by changes in ventricular mRNA, which increased about four-to sixfold. In contrast, protein levels in ventricles increased progressively over the 10-d treatment period. Ribonuclease protection analysis indicated that the relative amounts of fibronectin isoforms containing exons designated EIIIA and EIIIB increased during the progression of hypertropy. When cardiac hypertrophy was induced by mineralocorticoid and salt treatment, increases in ventricular fibronectin mRNA and protein and the induction of alternatively spliced forms of fibronectin were also observed. However, the extent and temporal pattern of fibronectin expression differed between the two experimental models. (J. Clin. Invest.

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Section: Resultsmentioning

confidence: 99%

Fibronectin expression in the normal and hypertrophic rat heart.

Mamuya¹,

Brecher²

1992

J. Clin. Invest.

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“…The observaReceived for publication 14 July 1980 and in revised form 29 September 1981. tion of Bishop and Melsen (8) that pulmonary artery banding in the cat produced myocardial necrosis and fibrosis, whereas neither was found in cats with congenital pulmonary valve stenosis, supports the latter possibility. Furthermore, it is clear that collagen concentration can increase, decrease, or remain unchanged during development of hypertrophy depending on the stimulus for increased growth (9) and that an inverse relationship between connective tissue and passive stiffness can be found under certain conditions (10). Therefore, we attempted to develop a model of pressure-induced hypertrophy in which hypertrophy developed more gradually than in the usual animal models and compared passive stiffness and the hydroxyproline response in these hearts.…”

Section: Introductionmentioning

confidence: 99%

Hydroxyproline and passive stiffness of pressure-induced hypertrophied kitten myocardium.

Williams¹,

Potter²,

Hern³

et al. 1982

J. Clin. Invest.

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A B S T R A C T Passive stiffness and hydroxyproline content of myocardium hypertrophied by pressureloading were determined in kittens 2, 8-16, and 24-52 wk after pulmonary artery banding, which initially elevated right ventricular systolic pressure by 10-15 mm Hg. Right ventricular mass increased by -75%, three-quarters of which occurred during the first 2 wk after banding. Passive stiffness was assessed from resting length-tension relations of isometrically contracting isolated right ventricular papillary muscles. Stiffness constants, a and B were determined from the relationship a = a(ee -1) where a = stress and e = Lagrangian strain. Elastic stiffness (dl/dE) was derived from: da/de = f#a + ,3a. Right ventricular hydroxyproline increased in proportion to muscle mass so that hydroxyproline concentration remained unchanged after banding. Both a, f, and elastic stiffnessstress relations were similar to values in nonbanded controls. Thus, we did not observe an increase in passive stiffness or hydroxyproline concentration of pressure-induced hypertrophied myocardium in contrast to most previous studies.

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“…45 It likewise does not appear with either the volume-overload hypertrophy associated with uninephrectomy and a high Na + diet, 45 a compensated arteriovenous fistula, 46 -51 chronic anemia, 52 atrial septal defect, 53 or the hypertrophy induced by chronic thyroxine administration. 52 - 54 In each of these latter circumstances the RAAS is not activated.…”

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confidence: 99%

Structural remodeling in hypertensive heart disease and the role of hormones.

1994

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In hypertension, the risk of adverse cardiovascular events, including heart failure, is increased in the presence of left ventricular hypertrophy. Morphological studies suggest that it is not the quantity but rather the quality, or structure, of myocardium that confers such risk. Iterations in tissue structure that appear in hypertensive heart disease include a remodeling of intramyocardial coronary arterioles, similar to that found in systemic organs, and a disproportionate accumulation of fibrillar collagen within their adventitia and neighboring interstitial space. Microscopic scars replacing necrotic cardiac myocytes are also evident. These expressions of fibrosis appear in the normotensive, nonhypertrophied right and hypertensive, hypertrophied left ventricles and are linked to the renin-angiotensin-aldosterone system. Cardiac myocyte growth, the major determinant of myocardial mass, is related to ventricular loading. Mechanisms responsible for the reactive and reparative fibrosis with renin-angiotensin-aldosterone system activation are under investigation. In vitro quantitative autoradiography has identified angiotensin II, aldosterone, T he appearance of symptomatic heart failure and adverse cardiovascular events, such as myocardial infarction, sudden cardiac death, and stroke, occur with increased frequency in patients with systemic hypertension. For years, the pathophysiologica] basis for such increased risk has been presumed to be solely related to elevated arterial pressure. More recently, emphasis in conferring risk has been placed on the structural remodeling of the cardiovasculature. For example, in patients with uncomplicated hypertension, risk has been linked to left ventricular hypertrophy (LVH). 13 Viewed not as a separate organ but as an integral component of the cardiovasculature, the heart and its intramyocardial coronary arteries and arterioles participate in a structural remodeling that involves systemic organs as well. 48 The remodeling of systemic arterioles accounts for hypertension. The heart in turn responds to enhanced ventricular loading with a hypertrophic growth of cardiac myocytes, and accordingly, left ventricular mass is increased. The diffuse nature of the structural remodeling process, involving the right and left ventricles and systemic organs, suggests a role for circulating substances or substances produced locally within cardiovascular tissue. In this connection, it is noteworthy that risk has also been linked to an activation of the renin-angiotensin-aldosterone system (RAAS). endothelin, and bradykinin receptors in the myocardium. A nonendothelial tissue angiotensin-converting enzyme, whose binding density is marked in the matrix of heart valves, adventitia, and sites of fibrosis, irrespective of its pathogenic basis, has also been found. This angiotensin-converting enzyme may be responsible for regulating local concentrations of angiotensin II and bradykinin that govern fibroblast collagen turnover. Based on a paradigm of discordant reciprocal regulation, in wh...

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The growth of the muscular and collagenous parts of the rat heart in various forms of cardiomegaly

Cited by 174 publications

References 22 publications

Fibronectin expression in the normal and hypertrophic rat heart.

Fibronectin expression in the normal and hypertrophic rat heart.

Hydroxyproline and passive stiffness of pressure-induced hypertrophied kitten myocardium.

Structural remodeling in hypertensive heart disease and the role of hormones.

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