Dynamics of nucleic acid and protein synthesis of the myocardium in compensatory hyperfunction and hypertrophy of the heart

Меерсон, Ф. З.; Alekhina, G.M.; Aleksandrov, P. N.; Bazardjan, A.G.

doi:10.1016/0002-9149(68)90118-5

Cited by 52 publications

(21 citation statements)

References 10 publications

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“…The studies of Meerson et al 40 show a decrease in the number of muscle nuclei per unit of myocardial area; this led them to conclude that there were insufficient amounts of DNA for adequate protein renewal. This also may imply that insufficient amounts of DNA for adequate renewal of cellular protein leads to a depression in contractile force.…”

Section: Discussionmentioning

confidence: 99%

“…Grove et al 38 reached a similar conclusion; rats with supravalvular aortic stenosis exhibited an increase in the total amount and concentration of hydroxyproline that was coincident with proliferation of connective tissue cells during the development of cardiac hypertrophy. In rats with aortic coarctation, Meerson et al 40 showed that a significant increment in connective tissue cells kept pace with the associated enlargement of myocardial cells. This increase in noncontractile fibrous tissue may be a potent factor in altering cardiac structure that leads to a decrease in ventricular compliance and depression of cardiac performance.…”

Section: Discussionmentioning

confidence: 99%

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Cardiac performance in rats with renal hypertension.

Averill

Ferrario

Tarazi³

et al. 1976

Circulation Research

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SUMMARY To evaluate cardiac performance in renal hypertension more precisely we determined cardiac function curves for 12 normotensive rats and 11 other rats with two-kidney Goldblatt hypertension. The hypertensive group (BP = 134 ± 8 mm Hg) showed significant cardiac hypertrophy (44 ± 1% increased ratio of heart weight to body weight, P < 0.01) and markedly increased left ventricular stroke work with a moderate but not significant increase in left ventricular end-diastolic pressure (LVEDP) (5.9 ± 0.8 vs. CARDIAC hypertrophy generally has been considered one of the principal long-term mechanisms of compensation for cardiac stress; 1 the increase in cardiac mass is believed to make the heart as strong a pump as it had been previously. It is known that the increase in contractile strength which follows hypertrophy is due to an increase in muscle mass and that the strength of individual muscle fibers remains unchanged or even may decrease slightly. 2 ' 7 The influence of myocardial hypertrophy on the performance of the hypertensive heart is of particular interest because cardii.c hypertrophy frequently accompanies arterial hypertension and it has been pointed out that early hypertension, in both man and animals, is associated with an increased cardiac output and signs of a hyperkinetic circulation. 8 " 11 The relationship of the increased cardiac output to the development of cardiac hypertrophy has yet to be investigated. Recent studies which show an increased cardiac contractility during the onset of renal hypertension 12 and the early development of cardiac hypertrophy in two forms of hypertension 13 -14 suggest a causal relationship between increased cardiac output and development of cardiac hypertrophy.With the advent of refinements in microtransducer technology it has become possible to accurately measure cardiac output and arterial and venous pressures in small mammals with and without arterial hypertension and thus evaluate cardiac performance in a precise manner. Further, correlation of hemodynamic alterations with biochemical changes which characterize the type of hypertrophy should open the way for a better understanding of cardiac mechanics. To our knowledge this has not been attempted before in hypertensive heart disease, nor is there direct information on the effects of cardiac hypertrophy on ventricular function curves (see Reference 15 for review). We therefore studied the functional link between the appearance of cardiac hypertrophy and the performance of the heart in rats with chronic renal hypertension. MethodsWe performed experiments on 20 normal Wistar rats and on 14 rats with sustained renal hypertension (average duration, 9 weeks; range, 6-22 weeks). All data presented are expressed as mean ± SE, unless stated otherwise for a specific value.Hypertension was produced by placing a silver clip with a 0.20-mm gap around the left renal artery; the contralateral kidney was left untouched. The rats were 10 weeks old at the time of constriction and average weight was 244 ± 11 g. All rats were housed...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Cardiac performance in rats with renal hypertension.

Averill

Ferrario

Tarazi³

et al. 1976

Circulation Research

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“…Therefore valvular disease should be treated earlier in order to limit the myocardial damage induced. The change in DNA/RNA ratio in the hypertrophied muscle fibers may be considered as a prognostic index for future myocardial function [7]. The electronmicroscopicai changes encountered in the myo cardium are not diagnostic or specific to the individual cases, but represent rather ultrastructural changes related to the functional state of the myo cardium and other factors such as anoxia [8] and electrolyte imbalance [9], These changes may be the underlying basis for further alterations of the muscle fiber, including degeneration and necrosis.…”

Section: Discussionmentioning

confidence: 99%

Morphological and Immunological Studies in Valvular Heart Surgery

Laufer¹,

Garcés²,

N³

et al. 1970

Pathobiology

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Light and electronmicroscopical studies were performed on myocardial samples, obtained from the atrium, papillary muscle, anterior wall of left ventricle and the operated valves. Degenerative verrucous endocardiosis and bacterial endocarditis were encountered but no histological signs of rheumatic activity were found. No specific diagnostic electronmicroscopical findings were present and the ultra-structural changes present included alterations in the mitochondria, an increase in the number of fat droplets, a focal increase in glycogen and focal muscle disruption and necrosis. The detection of anti-heart antibodies by indirect immunofluorescent studies and their possible relation to myocardial damage are discussed. In addition, the importance of myocardial changes, the presence of small myocardial scars and the increase in interstitial collagen tissue are reviewed in relation to myocardial function and it is suggested that they can be used as a prognostic index of myocardial function. It is also suggested that earlier operation of diseased valves be performed in order to prevent further myocardial damage and impairment of myocardial function.

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“…Increased DNA content of experimentally enlarged hearts has been correlated with increased heart weight and suggested to show increased cardiac cell numbers (Meerson et al, 1968;Morkin and Ashford, 1968;Grove et al, 1969a;Grimm et al, 1970). Grimm et al (1966) examined DNA and RNA concentrations insubdiaphragmatic aortic constriction and nonconstricted rats.…”

Section: Biochemical Changes In Adaptive Growth Of the Heartmentioning

confidence: 99%

“…Several studies utilized radioautographic techniques to follow 3 the incorporation of H-thymidine, and showed the increased DNA synthesis in the hypertrophied heart was confined to connective tissue cells (Meerson et al, 1968;Morkin and Ashford, 1968;Grove et al, 1969b).…”

Section: Biochemical Changes In Adaptive Growth Of the Heartmentioning

confidence: 99%

Myocardial adaptations to age and exercise in rats: responses to acute swimming and 1-iso-proterenol-induced myocardial ischemia

Fell

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Dynamics of nucleic acid and protein synthesis of the myocardium in compensatory hyperfunction and hypertrophy of the heart

Cited by 52 publications

References 10 publications

Cardiac performance in rats with renal hypertension.

Cardiac performance in rats with renal hypertension.

Morphological and Immunological Studies in Valvular Heart Surgery

Myocardial adaptations to age and exercise in rats: responses to acute swimming and 1-iso-proterenol-induced myocardial ischemia

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