Biomechanics of the Aging Lung Parenchyma

Suki, Bélâ; Bartolák‐Suki, Erzsébet

doi:10.1007/978-3-319-03970-1_5

Cited by 14 publications

(22 citation statements)

References 154 publications

(231 reference statements)

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“…13a, 34a) in the young and old alveolar/duct models was L m ϭ 236 and 342 m, respectively. This increase in L m with age is consistent with the literature (34).…”

Section: Discussionsupporting

confidence: 93%

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Evidence for age-dependent air-space enlargement contributing to loss of lung tissue elastic recoil pressure and increased shear modulus in older age

Subramaniam

Kumar

Tawhai

2017

Journal of Applied Physiology

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As a normal part of mature aging, lung tissue undergoes microstructural changes such as alveolar air-space enlargement and redistribution of collagen and elastin away from the alveolar duct. The older lung also experiences an associated decrease in elastic recoil pressure and an increase in specific tissue elastic moduli, but how this relates mechanistically to microstructural remodeling is not well-understood. In this study, we use a structure-based mechanics analysis to elucidate the contributions of age-related air-space enlargement and redistribution of elastin and collagen to loss of lung elastic recoil pressure and increase in tissue elastic moduli. Our results show that age-related geometric changes can result in reduction of elastic recoil pressure and increase in shear and bulk moduli, which is consistent with published experimental data. All elastic moduli were sensitive to the distribution of stiffness (representing elastic fiber density) in the alveolar wall, with homogenous stiffness near the duct and through the septae resulting in a more compliant tissue. The preferential distribution of elastic proteins around the alveolar duct in the healthy young adult lung therefore provides for a more elastic tissue. We use a structure-based mechanics analysis to correlate air-space enlargement and redistribution of elastin and collagen to age-related changes in the mechanical behavior of lung parenchyma. Our study highlights that both the cause (redistribution of elastin and collagen) and the structural effect (alveolar air-space enlargement) contribute to decline in lung tissue elastic recoil with age; these results are consistent with published data and provide a new avenue for understanding the mechanics of the older lung.

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“…13a, 34a) in the young and old alveolar/duct models was L m ϭ 236 and 342 m, respectively. This increase in L m with age is consistent with the literature (34).…”

Section: Discussionsupporting

confidence: 93%

“…13, 34a; a component of chronic obstructive pulmonary disease, which has age-related prevalence). Although many of the microstructural changes that accompany senescence are well-documented (4,18,34,38), how they contribute to the emergence of age-related decline in lung elastic properties at the macroscopic level remains unclear.…”

Section: New and Noteworthymentioning

confidence: 99%

Evidence for age-dependent air-space enlargement contributing to loss of lung tissue elastic recoil pressure and increased shear modulus in older age

Subramaniam

Kumar

Tawhai

2017

Journal of Applied Physiology

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“…For example, calcification of rib cartilages and changes in the chest wall geometry contribute to a decrease in chest wall compliance (Hirata et al 2015). Degeneration of elastic fibres in the lung reduces the static recoil pressure and contributes to 'senile' hyperinflation (Suki & Bartolák-Suki, 2015). Respiratory muscle fibres decrease in number, function at a shorter disadvantageous length, convert from type II to weaker fatigue-resistant type I fibres and undergo progressive denervation (Biolo et al 2014).…”

Section: Bps In Quiet Breathingmentioning

confidence: 99%

Inspiratory pre‐motor potentials during quiet breathing in ageing and chronic obstructive pulmonary disease

Nguyen

Boswell‐Ruys

McBain

et al. 2018

The Journal of Physiology

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A cortical contribution to breathing is determined by the presence of a Bereitschaftspotential, a low amplitude negativity in the averaged electroencephalographic (EEG) signal, which begins ∼1 s before inspiration. It occurs in healthy individuals when external inspiratory loads to breathing are applied. In chronic obstructive pulmonary disease (COPD), changes in the lung, chest wall and respiratory muscles produce an internal inspiratory load. We hypothesized that there would be a cortical contribution to quiet breathing in COPD and that a cortical contribution to breathing with an inspiratory load would be linked to dyspnoea, a major symptom of COPD. EEG activity was analysed in 14 participants with COPD (aged 57-84 years), 16 healthy age-matched (57-87 years) and 15 young (18-26 years) controls during quiet breathing and inspiratory loading. The presence of Bereitschaftspotentials, from ensemble averages of EEG epochs at Cz and FCz, were assessed by blinded assessors. Dyspnoea was rated using the Borg scale. The incidence of a cortical contribution to quiet breathing was significantly greater in participants with COPD (6/14) compared to the young (0/15) (P = 0.004) but not the age-matched controls (6/16) (P = 0.765). A cortical contribution to inspiratory loading was associated with higher Borg ratings (P = 0.007), with no effect of group (P = 0.242). The data show that increased age, rather than COPD, is associated with a cortical contribution to quiet breathing. A cortical contribution to inspiratory loading is associated with more severe dyspnoea. We propose that cortical mechanisms may be engaged to defend ventilation with dyspnoea as a consequence.

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“…G is an inverse measure of compliance in the parenchymal lung tissue and its increase in ALI, related to septal edema formation, has been shown previously [29]. Hysteresis might increase due to changes in tissue resistance and elastance or due to changes in surfactant composition [30,31]. We further analyzed the septal composition on the ultrastructural level to characterize changes in septal tissue composition, including cells and ECM.…”

Section: Discussionmentioning

confidence: 94%

miR-21-KO Alleviates Alveolar Structural Remodeling and Inflammatory Signaling in Acute Lung Injury

Jansing

Fiedler

Pich

et al. 2020

IJMS

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Acute lung injury (ALI) is characterized by enhanced permeability of the air–blood barrier, pulmonary edema, and hypoxemia. MicroRNA-21 (miR-21) was shown to be involved in pulmonary remodeling and the pathology of ALI, and we hypothesized that miR-21 knock-out (KO) reduces injury and remodeling in ALI. ALI was induced in miR-21 KO and C57BL/6N (wildtype, WT) mice by an intranasal administration of 75 µg lipopolysaccharide (LPS) in saline (n = 10 per group). The control mice received saline alone (n = 7 per group). After 24 h, lung function was measured. The lungs were then excised for proteomics, cytokine, and stereological analysis to address inflammatory signaling and structural damage. LPS exposure induced ALI in both strains, however, only WT mice showed increased tissue resistance and septal thickening upon LPS treatment. Septal alterations due to LPS exposure in WT mice consisted of an increase in extracellular matrix (ECM), including collagen fibrils, elastic fibers, and amorphous ECM. Proteomics analysis revealed that the inflammatory response was dampened in miR-21 KO mice with reduced platelet and neutrophil activation compared with WT mice. The WT mice showed more functional and structural changes and inflammatory signaling in ALI than miR-21 KO mice, confirming the hypothesis that miR-21 KO reduces the development of pathological changes in ALI.

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Biomechanics of the Aging Lung Parenchyma

Cited by 14 publications

References 154 publications

Evidence for age-dependent air-space enlargement contributing to loss of lung tissue elastic recoil pressure and increased shear modulus in older age

Evidence for age-dependent air-space enlargement contributing to loss of lung tissue elastic recoil pressure and increased shear modulus in older age

Inspiratory pre‐motor potentials during quiet breathing in ageing and chronic obstructive pulmonary disease

miR-21-KO Alleviates Alveolar Structural Remodeling and Inflammatory Signaling in Acute Lung Injury

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