Capillaries and Muscle Fibres in the Heart of Old Rats

Rakusan, K; Poupa, O

doi:10.1159/000211244

Cited by 42 publications

(5 citation statements)

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“…In contrast to senescent animals [10]–[13] we found no increase in fibrosis of older patients, in agreement with previous studies in humans [19], [57], and no effect of age on capillary length density and diffusion radius, in agreement with the autopsy study of Roberts and Wearn [18]. Moreover, the lack of effect of age on coronary arteriolar dimensions was in agreement with studies of senescent beagles [11].…”

Section: Discussionsupporting

confidence: 92%

“…Heart failure, with either reduced or preserved ejection fraction, is associated with abnormalities of myocardial structure and microvasculature including increased fibrosis, cardiomyocyte hypertrophy and reduced microvascular density [5]–[9], and animal models suggest that these abnormalities precede the development of heart failure in older age. Senescent animals have reduced cardiomyocyte number, hypertrophy of surviving cardiomyocytes, increased cardiac fibrosis, reduced capillary density and increased diffusion radius [10]–[13]. In addition, advanced glycation end-products (AGEs) are proposed to contribute to the increased myocardial stiffening of aging by cross-linking collagen and elastin and promoting collagen accumulation [14], and by promoting inflammation and oxidative stress mediated by the receptor for AGEs (RAGE) [15].…”

Section: Introductionmentioning

confidence: 99%

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Diastolic Dysfunction of Aging Is Independent of Myocardial Structure but Associated with Plasma Advanced Glycation End-Product Levels

et al. 2012

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BackgroundHeart failure is associated with abnormalities of myocardial structure, and plasma levels of the advanced glycation end-product (AGE) Nε-(carboxymethyl)lysine (CML) correlate with the severity and prognosis of heart failure. Aging is associated with diastolic dysfunction and increased risk of heart failure, and we investigated the hypothesis that diastolic dysfunction of aging humans is associated with altered myocardial structure and plasma AGE levels.MethodsWe performed histological analysis of non-ischemic left ventricular myocardial biopsies and measured plasma levels of the AGEs CML and low molecular weight fluorophores (LMWFs) in 26 men undergoing coronary artery bypass graft surgery who had transthoracic echocardiography before surgery. None had previous cardiac surgery, myocardial infarction, atrial fibrillation, or heart failure.ResultsThe patients were aged 43–78 years and increasing age was associated with echocardiographic indices of diastolic dysfunction, with higher mitral Doppler flow velocity A wave (r = 0.50, P = 0.02), lower mitral E/A wave ratio (r = 0.64, P = 0.001), longer mitral valve deceleration time (r = 0.42, P = 0.03) and lower early diastolic peak velocity of the mitral septal annulus, e’ (r = 0.55, P = 0.008). However, neither mitral E/A ratio nor mitral septal e’ was correlated with myocardial total, interstitial or perivascular fibrosis (picrosirius red), immunostaining for collagens I and III, CML, and receptor for AGEs (RAGE), cardiomyocyte width, capillary length density, diffusion radius or arteriolar dimensions. Plasma AGE levels were not associated with age. However, plasma CML levels were associated with E/A ratio (r = 0.44, P = 0.04) and e’ (r = 0.51, P = 0.02) and LMWF levels were associated with E/A ratio (r = 0.49, P = 0.02). Moreover, the mitral E/A ratio remained correlated with plasma LMWF levels in all patients (P = 0.04) and the mitral septal e’ remained correlated with plasma CML levels in non-diabetic patients (P = 0.007) when age was a covariate.ConclusionsDiastolic dysfunction of aging was independent of myocardial structure but was associated with plasma AGE levels.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Diastolic Dysfunction of Aging Is Independent of Myocardial Structure but Associated with Plasma Advanced Glycation End-Product Levels

et al. 2012

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“…As it was demonstrated experimentally, hypodynamy results in a loss of mitochondrial activity [47], Additional secondary factors have to be considered as possible causes of a reduced availability of oxygen to the tissue, e.g. diminution of the number of capillaries [52], of number of erythrocytes, or of oxygen-bind ing capacity of hemoglobin, and any deterioration within the oxygen up take system from lung to tissue. However, changes if any, described up to now for these systems are small and cannot account for the cell's deterio rated respiratory function.…”

Section: Discussionmentioning

confidence: 98%

Ageing Changes in Mammalian Skeletal Muscle

Ermini¹

1976

Gerontology

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In the course of ageing, biochemical characteristics of mammalian skeletal muscle are shown to become altered mainly within the system of energy metabolism. The enzymatic behaviour of myofibrillar proteins remains virtually unchanged throughout life, but a gradual loss of fibres causes a decrease in muscular strength. Working capacity, however, in terms of prolonged muscular work is considerably reduced with age, because of a less efficient energy metabolism. Enzymes, particularly of the Krebs cycle, show diminished specific activities, and consequently, ATP and phosphocreatine concentrations are lowered. Possible primary and secondary factors responsible for these changes are discussed.

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“…Since these anatomical variables are major determinants of wall stress, the extent of elevation in mural diastolic stress with aging was not significantly different in the two sides of the heart. In contrast, other significant components of the aging process, including depression in muscle mechanical behavior (Lakatta and Yin, 1982;Capasso et al, 19891, reduc-tions in capillary luminal volume and capillary numerical density (Rakusan and Poupa, 1964;Tomanek, 1970;Olivetti et al, 1990), and magnitude of myocyte cell loss (Anversa et al, 19861, affect first the left myocardium and subsequently the right myocardium. However, impairment of coronary vascular reserve and resistance develops concomitantly in the two ventricles (Hachamovitch et al, 1989).…”

Section: Discussionmentioning

confidence: 99%

Myocyte DNA synthesis with aging: Correlation with ventricular loading in rats

Capasso

Bruno

Zhang

et al. 1993

Journal Cellular Physiology

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To determine whether the detrimental mechanical and anatomical changes that occur biventricularly with aging are associated with activation of DNA synthesis, flow cytometric analysis was performed on myocyte nuclei prepared from the left and right ventricles of rats at 4, 12, 20, and 29 months of age. Heart weight increased significantly with age, and this growth adaptation was associated with the development of left ventricular failure and right ventricular dysfunction. These phenomena were coupled with marked elevations in diastolic wall stress and increases in the percentage of myocyte nuclei in S+G2M in both ventricles. Linear regression analyses revealed a direct correlation between the fraction of myocytes that entered the cell cycle and diastolic pressure and wall stress. An inverse relation was found between the percentage of myocyte nuclei in S+G2M and +dP/dt and systolic wall stress. Thus the depression of hemodynamic performance coupled with alterations in the loading conditions contributes, at least in part, to increased DNA synthesis in cardiac myocytes with age.

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Capillaries and Muscle Fibres in the Heart of Old Rats

Cited by 42 publications

References 4 publications

Diastolic Dysfunction of Aging Is Independent of Myocardial Structure but Associated with Plasma Advanced Glycation End-Product Levels

Diastolic Dysfunction of Aging Is Independent of Myocardial Structure but Associated with Plasma Advanced Glycation End-Product Levels

Ageing Changes in Mammalian Skeletal Muscle

Myocyte DNA synthesis with aging: Correlation with ventricular loading in rats

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