Age-Dependent Changes of Collagen and Elastin Content in Human Aorta and Pulmonary Artery

Hosoda, Yasuhiro; Kawano, Koichi; Yamasawa, Fumihiro; Ishii, Toshiharu; Shibata, Tetsuichi; Inayama, Seiichi

doi:10.1177/000331978403501001

Cited by 100 publications

(76 citation statements)

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“…However, r 2 =0.5 means that 50% of the difference in distensibility was accounted for by age. The present data are in line with a number of earlier observations, obtained both in vitro and in vivo [9,10]. PASIERSKI et al [12], however, employing the conventional ultrasound M-mode technique for measuring vessel diameter, found that the elastic modulus (the ratio of pulmonary arterial pressure to vessel wall strain) was independent of age, and was related only to pulmonary arterial pressure.…”

Section: Influence Of Agesupporting

confidence: 93%

mentioning

confidence: 96%

“…The age dependence of pulmonary arterial wall distensibility is another controversial issue. Although in vitro studies have shown that the pulmonary arterial wall stiffens with age [9,10], in vivo studies have produced equivocal results; a negative correlation between pulmonary compliance and age was reported in one study [11] but no such relation was found in another [12].In view of the above uncertainties, the relationship between Dst and Ddyn of the right main pulmonary artery and its age dependence was studied. Ddyn was determined from the pressure/diameter relationship during the cardiac cycle, whereas static (or, rather, quasistatic) distensibility was determined using changes in mean pulmonary artery pressure (MPAP) and diameter during physical exercise.…”

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confidence: 99%

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Assessment of the viscosity of the pulmonary artery wall

et al. 2000

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Large artery wall viscosity reduces the efficiency of heart/vessel coupling. The aim of the present study was to assess pulmonary artery wall viscosity through comparison of the static (Dst) and dynamic distensibility (Ddyn) of the vessel wall.Right pulmonary artery pressure and diameter was measured in 13 patients and eight healthy volunteers. Ddyn was calculated as the relative change in end-diastolic diameter induced by the pressure pulse, and Dst as the relative change in mean diameter induced by the change in mean pressure during steady-state exercise.Dst The arterial wall responds to stress through both elastic and viscous behaviour, the former being related to the elastin and the latter to the collagen and smooth muscle content of the vessel wall [1,2]. During systole, the elastic behaviour of the arterial wall allows its diameter to increase proportionally to pressure; in the case of a purely elastic arterial wall, the total amount of energy stored would be released during diastole. In reality, however, part of the energy that corresponds to viscous deformation is dissipated within the arterial wall. Wall viscosity reduces the efficiency of heart/vessel coupling, and may place extra load on the ventricle [3].Wall viscosity is responsible for the difference that exists between the static (Dst) and dynamic distensibility (Ddyn) of a given vessel [1,2,4,5]. Under static conditions, the change in diameter in response to a given change in distending pressure is determined only by the elastic properties of the vessel wall. Under dynamic conditions, however, when changes in pressure are pulsatile and the time available for distension is limited, wall viscosity impedes distension, resulting in less change in diameter for the same change in pressure [6]. The greater the wall viscosity, the greater the difference between Dst and Ddyn. Dst has been found to be considerably higher than Ddyn in systemic arteries, the difference being accounted for by wall viscosity [1,2,4,5].Information on pulmonary artery wall viscosity is limited and controversial. In the perfused dog lungs, the slope of the static curve relating volume to pressure (i.e. lung compliance) was found to be 1.5 times steeper than that of the dynamic curve [7], indicating considerable vessel wall viscosity. In humans, no direct comparison of Dst and Ddyn of the pulmonary artery has been made, but the close similarity of pressure and diameter curves recorded from the pulmonary artery has been taken as a sign of low vessel wall viscosity [8]. The age dependence of pulmonary arterial wall distensibility is another controversial issue. Although in vitro studies have shown that the pulmonary arterial wall stiffens with age [9,10], in vivo studies have produced equivocal results; a negative correlation between pulmonary compliance and age was reported in one study [11] but no such relation was found in another [12].In view of the above uncertainties, the relationship between Dst and Ddyn of the right main pulmonary artery and its age dependence was ...

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Section: Influence Of Agesupporting

confidence: 93%

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confidence: 96%

mentioning

confidence: 99%

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Assessment of the viscosity of the pulmonary artery wall

et al. 2000

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“…9,10,32 For example, the elastin/collagen ratio of the aorta is of 1.5, whereas that of the femoral artery is 0.5 (see ref. 33). This ratio is also altered during arterial aging and by the atherosclerotic process, and fragmentation of the elastic fiber network leads to premature recruitment of the most rigid collagen fibers.…”

Section: Discussionmentioning

confidence: 99%

Assessment of aortic stiffness by local and regional methods

et al. 2011

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The stiffness of large arteries has an important role in cardiovascular hemodynamics. Aortic stiffness (AoStiff) can be assessed non-invasively with regional and local methods. In this paper, we compared these two techniques for evaluating AoStiff. Our subjects comprised of 118 consecutive patients (85 men, mean age: 49 ± 14 years). We evaluated regional AoStiff with carotid-femoral pulse wave velocity (PWV) measured with a tonometric technique and by bioelectrical impedance (BI) wave velocity (IWV). The local AoStiff was calculated from BI signals recorded at the chest. We used glyceryl trinitrate (GTN) to test the effect of peripheral vasodilatation on both methods in a subgroup of 52 patients (37 men, mean age: 52 ± 11 years). We found a significant correlation between IWV and PWV measurements (r¼0.88, Po0.0001) as well as between AoStiff and PWV measurements (r¼0.75, Po0.0001). GTN administration decreased mean arterial blood pressure by 4% (95% confidence interval: 2-8%, P¼0.002) without significant changes in AoStiff and regional IWV. Local AoStiff is correlated with regional measurements and is not influenced by changes in arterial pressure because of systemic peripheral vasodilatation.

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“…Arterial collagen concentration has been reported to: steadily increase, to increase only after the age of 50 and to remain unchanged with age (Cattell et al 1996;Hosoda et al 1984;Maurel et al 1987). Although elastin concentration in ageing arteries has been reported to decrease (Hosoda et al 1984;Maurel et al 1987), in the specific case of normotensive individuals, aortic elastin concentration appears to increase (Cattell et al 1996). Cattell and co-workers highlight the need to distinguish between changes in the absolute amount of a tissue component versus changes in its concentration (Cattell et al 1996).…”

Section: Vascularmentioning

confidence: 99%

Tissue elasticity and the ageing elastic fibre

Sherratt

2009

AGE

270

189

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The ability of elastic tissues to deform under physiological forces and to subsequently release stored energy to drive passive recoil is vital to the function of many dynamic tissues. Within vertebrates, elastic fibres allow arteries and lungs to expand and contract, thus controlling variations in blood pressure and returning the pulmonary system to a resting state. Elastic fibres are composite structures composed of a cross-linked elastin core and an outer layer of fibrillin microfibrils. These two components perform distinct roles; elastin stores energy and drives passive recoil, whilst fibrillin microfibrils direct elastogenesis, mediate cell signalling, maintain tissue homeostasis via TGFβ sequestration and potentially act to reinforce the elastic fibre. In many tissues reduced elasticity, as a result of compromised elastic fibre function, becomes increasingly prevalent with age and contributes significantly to the burden of human morbidity and mortality. This review considers how the unique molecular structure, tissue distribution and longevity of elastic fibres pre-disposes these abundant extracellular matrix structures to the accumulation of damage in ageing dermal, pulmonary and vascular tissues. As compromised elasticity is a common feature of ageing dynamic tissues, the development of strategies to prevent, limit or reverse this loss of function will play a key role in reducing age-related morbidity and mortality.

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Age-Dependent Changes of Collagen and Elastin Content in Human Aorta and Pulmonary Artery

Cited by 100 publications

References 11 publications

Assessment of the viscosity of the pulmonary artery wall

Assessment of the viscosity of the pulmonary artery wall

Assessment of aortic stiffness by local and regional methods

Tissue elasticity and the ageing elastic fibre

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