Hypertrophied Non-Failing Rat Heart: PARTIAL BIOCHEMICAL CHARACTERIZATION

Dart, Charles H.; Holloszy, John O.

doi:10.1161/01.res.25.3.245

Cited by 37 publications

(5 citation statements)

References 34 publications

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“…A statistically significant heart weight increase was observed already after 2 days. This value agrees well with the results of the studies on surgically induced pressure or volume overload (8,24). The time course of the regression of the hypertrophy shows great variations from complete return to normal level within 14 days after the termination of swimming training (17) to unchanged heart weights 78 days after the closure of aortacaval fistula (28).…”

Section: Introductionsupporting

confidence: 92%

Selected enzyme activities in mouse cardiac muscle during training and terminated training

1984

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We studied the effects of running-training, heavy exercise and termination of training on the heart weight, the ratio heart to body weight and the cardiac muscle activities of actomyosin ATPase, citrate synthase, succinate dehydrogenase, cytochrome c oxidase, malate dehydrogenase, adenylate kinase and beta-glucuronidase with adult male NMRI-mice. Stable hypertrophy (6-7%), estimated by the ratio heart or ventricle weight to body weight, was achieved by 28 exercises and it was dependent on the running speed (20 vs. 25 m X min-1). The withdrawal of training for 5-61 days did not permanently decrease the heart weight or the heart to body weight ratio to the level of sedentary controls. The activity of enzymes of energy metabolism or actomyosin ATPase were not affected by training, heavy exercise or terminated training. beta-glucuronidase activity slightly (20-25%) increased in the trained animals and remained at a higher level during the period of terminated training. The results suggest that the capacity for aerobic metabolism of normal mice heart is sufficient to meet the enhanced demand for ATP imposed by running-training and that the heart enlargement occurs in equal proportions with the enzymatic potential of the cardiac tissue.

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Section: Introductionsupporting

confidence: 92%

Selected enzyme activities in mouse cardiac muscle during training and terminated training

1984

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“…Chronic volume overload in small animal models reproduces the pathologies observed in patients with mitral valve regurgitation, which typically increase diastolic wall stress and cause eccentric cardiac hypertrophy 12 . Cardiac volume overload is accomplished in rodents by creating a surgical aorto-caval shunt and has been reported for rats 54 , 55 and mice 12 . Volume overload in rats initially decreases LV function.…”

Section: Small Animal Models Of Hfrefmentioning

confidence: 94%

Small animal models of heart failure

Riehle

Bauersachs

2019

Cardiovascular Research

169

150

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Heart disease is a major cause of death worldwide with increasing prevalence, which urges the development of new therapeutic strategies. Over the last few decades, numerous small animal models have been generated to mimic various pathomechanisms contributing to heart failure (HF). Despite some limitations, these animal models have greatly advanced our understanding of the pathogenesis of the different aetiologies of HF and paved the way to understanding the underlying mechanisms and development of successful treatments. These models utilize surgical techniques, genetic modifications, and pharmacological approaches. The present review discusses the strengths and limitations of commonly used small animal HF models, which continue to provide crucial insight and facilitate the development of new treatment strategies for patients with HF.

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“…This sequence of initially increased and subsequently decreased relative mitochondrial mass appears to be the characteristic response of the enlarging myocardium to an acute pressure overload. When the heart enlarges secondary to a gradually imposed pressure overload (Wollenberger and Schultze, 1962;Wollenberger et al, 1966) or to volume overload (Dart and Holloszy, 1969;Oscai et al, 1971), such changes are not detected.…”

Section: Mitochondrial Mass and Cardiac Hypertrophymentioning

confidence: 99%

Changes in mitochondrial DNA in cardiac hypertrophy in the rat.

Rajamanickam¹,

Merten²,

Kwiatkowska-Patzer³

et al. 1979

Circulation Research

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SUMMARY We studied DNA (mtDNA) replication in adult female rat hearts undergoing hypertrophy secondary to constriction of the ascending aorta. MtDNA was measured in isolated mitochondria by a fiuorometric method adapted for that purpose. The conditions for removal of contaminating nuclear DNA were developed, and the purity of the mtDNA was assessed from its molecular conformation (open and closed circles) and by renaturation-kinetic analysis. The mtDNA concentration in mitochondria, expressed as micrograms of DNA per milligram of mitochondrial protein, increased 2, 4, and 7 days postoperatively by 21, 73, and 98%, respectively. Similar results were obtained when mtDNA was expressed per nanomole of cytochrome a. The population of replicative intermediates of mtDNA was analyzed by electron microscopy. In normal hearts, we observed molecular forms characteristic of animal mtDNA, such as circular monomers and dimers, catenated molecules, D-loops, expanded Dloops, and gapped molecules. D-loop frequency, which was near 50% in the mtDNA of control hearts, was markedly reduced to 5-7% in hypertrophying hearts. This result indicates that the increase in replicative flux of mtDNA is associated with the removal of a block in the conversion of D-loops to other intermediates. Ore Res. 46: 1979 IT is now well established that increased tension in the ventricular wall is correlated with increased metabolic activity of the heart. It is also known that the energy requirement of the myocardium is met completely by aerobic metabolism during both rest and strenuous activity (Neely and Morgan, 1974). This dependence of the myocardium on oxidative processes is reflected by the high content of mitochondria, which occupy 35% of the cardiac cell volume (Page et al., 1972).The increased requirement for ATP during acute work overload is met effectively by the respiratory control mechanism: the accumulating ADP stimulates oxidative phosphorylation. If the hemodynamic overload is sustained, however, the capacity of the existing contractile and energy-producing apparatus is exceeded, and a second adaptive process, cardiac growth, is activated. This adaptive growth is reflected in increased incorporation of labeled amino acids into cardiac subcellular fractions, including mitochondria, as measured both in vivo (Zak and Fischman, 1971) and in vitro (Shahab and Wollenberger, 1970). Quantitative electronmicroscopic analysis (Page et al., 1972) and measurements of mitochondrial cytochromes and respiratory enzymes (Albin et al., 1973) indicate that, in early hypertrophy, mitochondria accumulate in preference to other organelles. Thus, the study of processes leading to mitochondrial proliferation may provide clues about the still elusive feedback mechanism that couples hemodynamic load with biosynthetic pathways. In this respect, the report of Meerson and Pomoinitsky (1972) that the amount of mtDNA, expressed per unit of mitochondrial protein, is increased strikingly after aortic constriction in the rat is of great interest. The mtDNA concentra...

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Hypertrophied Non-Failing Rat Heart: PARTIAL BIOCHEMICAL CHARACTERIZATION

Cited by 37 publications

References 34 publications

Selected enzyme activities in mouse cardiac muscle during training and terminated training

Selected enzyme activities in mouse cardiac muscle during training and terminated training

Small animal models of heart failure

Changes in mitochondrial DNA in cardiac hypertrophy in the rat.

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