scholarly journals Investigating biases in the measurement of apparent alveolar septal wall thickness with hyperpolarized 129Xe MRI

2020 ◽  
Vol 84 (6) ◽  
pp. 3027-3039
Author(s):  
Kai Ruppert ◽  
Faraz Amzajerdian ◽  
Yi Xin ◽  
Hooman Hamedani ◽  
Luis Loza ◽  
...  
Keyword(s):  
Wall Thickness ◽  
Septal Wall ◽  
Hyperpolarized 129Xe ◽  
Septal Wall Thickness

scholarly journals The role of inducible nitric oxide synthase for interstitial remodeling of alveolar septa in surfactant protein D-deficient mice

2015 ◽  
Vol 309 (9) ◽  
pp. L959-L969 ◽  
Author(s):  
Lars Knudsen ◽  
Elena N. Atochina-Vasserman ◽  
Christopher B. Massa ◽  
Bastian Birkelbach ◽  
Chang-Jiang Guo ◽  
...  
Keyword(s):  
Surface Area ◽  
Wall Thickness ◽  
Alveolar Epithelium ◽  
Surfactant Protein ◽  
Lung Mechanics ◽  
Surfactant Protein D ◽  
Wall Thickening ◽  
Interstitial Tissue ◽  
Septal Wall ◽  
Septal Wall Thickness

Surfactant protein D (SP-D) modulates the lung's immune system. Its absence leads to NOS2-independent alveolar lipoproteinosis and NOS2-dependent chronic inflammation, which is critical for early emphysematous remodeling. With aging, SP-D knockout mice develop an additional interstitial fibrotic component. We hypothesize that this age-related interstitial septal wall remodeling is mediated by NOS2. Using invasive pulmonary function testing such as the forced oscillation technique and quasistatic pressure-volume perturbation and design-based stereology, we compared 29-wk-old SP-D knockout (Sftpd−/−) mice, SP-D/NOS2 double-knockout (DiNOS) mice, and wild-type mice (WT). Structural changes, including alveolar epithelial surface area, distribution of septal wall thickness, and volumes of septal wall components (alveolar epithelium, interstitial tissue, and endothelium) were quantified. Twenty-nine-week-old Sftpd−/− mice had preserved lung mechanics at the organ level, whereas elastance was increased in DiNOS. Airspace enlargement and loss of surface area of alveolar epithelium coexist with increased septal wall thickness in Sftpd−/− mice. These changes were reduced in DiNOS, and compared with Sftpd−/− mice a decrease in volumes of interstitial tissue and alveolar epithelium was found. To understand the effects of lung pathology on measured lung mechanics, structural data were used to inform a computational model, simulating lung mechanics as a function of airspace derecruitment, septal wall destruction (loss of surface area), and septal wall thickening. In conclusion, NOS2 mediates remodeling of septal walls, resulting in deposition of interstitial tissue in Sftpd−/−. Forward modeling linking structure and lung mechanics describes the complex mechanical properties by parenchymatous destruction (emphysema), interstitial remodeling (septal wall thickening), and altered recruitability of acinar airspaces.

scholarly journals Maladaptive Changes Associated With Cardiac Aging Are Sex-Specific and Graded by Frailty and Inflammation in C57BL/6 Mice

2020 ◽  
Author(s):  
Alice E Kane ◽  
Elise S Bisset ◽  
Stefan Heinze-Milne ◽  
Kaitlyn M Keller ◽  
Scott A Grandy ◽  
...  
Keyword(s):  
Ejection Fraction ◽  
Wall Thickness ◽  
Structure And Function ◽  
Cardiac Structure ◽  
Septal Wall ◽  
Serum Cytokines ◽  
Lv Mass ◽  
Septal Wall Thickness ◽  
Cardiac Structure And Function ◽  
And Function

Abstract We investigated whether late-life changes in cardiac structure and function were related to high levels of frailty and inflammation in male and female mice. Frailty (frailty index), ventricular structure/function (echocardiography), and serum cytokines (multiplex immunoassay) were measured in 16- and 23-month-old mice. Left ventricular (LV) mass and septal wall thickness increased with age in both sexes. Ejection fraction increased with age in males (60.4 ± 1.4 vs 68.9 ± 1.8%; p < .05) but not females (58.8 ± 2.5 vs 62.6 ± 2.4%). E/A ratios declined with age in males (1.6 ± 0.1 vs 1.3 ± 0.1; p < .05) but not females (1.4 ± 0.1 vs 1.3 ± 0.1) and this was accompanied by increased ventricular collagen levels in males. These changes in ejection fraction (r = 0.52; p = .01), septal wall thickness (r = 0.59; p = .002), E/A ratios (r = −0.49; p = .04), and fibrosis (r = 0.82; p = .002) were closely graded by frailty scores in males. Only septal wall thickness and LV mass increased with frailty in females. Serum cytokines changed modestly with age in both sexes. Nonetheless, in males, E/A ratios, LV mass, LV posterior wall thickness, and septal wall thickness increased as serum cytokines increased (eg, IL-6, IL-3, IL-1α, IL-1β, tumor necrosis factor-α, eotaxin, and macrophage inflammatory protein-1α), while ejection fraction declined with increasing IL-3 and granulocyte-macrophage colony stimulating factor. Cardiac outcomes were not correlated with inflammatory cytokines in females. Thus, changes in cardiac structure and function in late life are closely graded by both frailty and markers of inflammation, but this occurs primarily in males. This suggests poor overall health and inflammation drive maladaptive changes in older male hearts, while older females may be resistant to these adverse effects of frailty.

scholarly journals Significance of NT-proBNP and High-Sensitivity Troponin in Friedreich Ataxia

2020 ◽  
Vol 9 (6) ◽  
pp. 1630
Author(s):  
Lise Legrand ◽  
Carole Maupain ◽  
Marie-Lorraine Monin ◽  
Claire Ewenczyk ◽  
Richard Isnard ◽  
...  
Keyword(s):  
Wall Thickness ◽  
Plasma Levels ◽  
High Sensitivity ◽  
Left Ventricular ◽  
Filling Pressure ◽  
Left Ventricular Filling Pressure ◽  
Septal Wall ◽  
Septal Wall Thickness ◽  
Ventricular Filling Pressure ◽  
Ventricular Filling

Background: Friedreich’s ataxia (FA) is a rare autosomal recessive mitochondrial disease resulting of a triplet repeat expansion guanine-adenine-adenine (GAA) in the frataxin (FXN) gene, exhibiting progressive cerebellar ataxia, diabetes and cardiomyopathy. We aimed to determine the relationship between cardiac biomarkers, serum N-terminal pro-brain natriuretic peptide (NT-proBNP), and serum cardiac high-sensitivity troponin (hsTnT) concentrations, and the extent of genetic abnormality and cardiac parameters. Methods: Between 2013 and 2015, 85 consecutive genetically confirmed FA adult patients were prospectively evaluated by measuring plasma hsTnT and NT-proBNP concentrations, electrocardiogram, and echocardiography. Results: The 85 FA patients (49% women) with a mean age of 39 ± 12 years, a mean disease onset of 17 ± 11 years had a mean SARA (Scale for the Assessment and Rating of Ataxia) score of 26 ± 10. The median hsTnT concentration was 10 ng/L (3 to 85 ng/L) and 34% had a significant elevated hsTnT ≥ 14 ng/L. Increased septal wall thickness was associated with increased hsTnT plasma levels (p < 0.001). The median NT-proBNP concentration was 31 ng/L (5 to 775 ng/L) and 14% had significant elevated NT-proBNP ≥ 125 ng/L. Markers of increased left ventricular filling pressure (trans mitral E/A and lateral E/E’ ratio) were associated with increased NT-proBNP plasma levels (p = 0.01 and p = 0.01). Length of GAA or the SARA score were not associated with hsTnT or NT-proBNP plasma levels. Conclusion: hsTnT was increased in 1/3 of the adult FA and associated with increased septal wall thickness. Increased NT-proBNP remained a marker of increased left ventricular filling pressure. This could be used to identify patients that should undergo a closer cardiac surveillance.

scholarly journals Surfactant replacement therapy reduces acute lung injury and collapse induration-related lung remodeling in the bleomycin model

2017 ◽  
Vol 313 (2) ◽  
pp. L313-L327 ◽  
Author(s):  
Lilian Steffen ◽  
Clemens Ruppert ◽  
Heinz-Gerd Hoymann ◽  
Manuela Funke ◽  
Simone Ebener ◽  
...  
Keyword(s):  
Surface Tension ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Replacement Therapy ◽  
Wall Thickness ◽  
Inflammatory Markers ◽  
Septal Wall ◽  
Surfactant Replacement Therapy ◽  
Septal Wall Thickness ◽  
Surfactant Dysfunction

Bleomycin-induced lung injury leads to surfactant dysfunction and permanent loss of alveoli due to a remodeling process called collapse induration. Collapse induration also occurs in acute interstitial lung disease and idiopathic pulmonary fibrosis in humans. We hypothesized that surfactant dysfunction aggravates lung injury and early remodeling resulting in collapse induration within 7 days after lung injury. Rats received bleomycin to induce lung injury and either repetitive surfactant replacement therapy (SRT: 100 mg Curosurf/kg BW = surf group) or saline (0.9% NaCl = saline group). After 3 (D3) or 7 (D7) days, invasive pulmonary function tests were performed to determine tissue elastance (H) and static compliance (Cst). Bronchoalveolar lavage (BAL) was taken for surfactant function, inflammatory markers, and protein measurements. Lungs were fixed by vascular perfusion for design-based stereology and electron microscopic analyses. SRT significantly improved minimum surface tension of alveolar surfactant as well as H and Cst at D3 and D7. At D3 decreased inflammatory markers including neutrophilic granulocytes, IL-1β, and IL-6 correlated with reduced BAL-protein levels after SRT. Numbers of open alveoli were significantly increased at D3 and D7 in SRT groups whereas at D7 there was also a significant reduction in septal wall thickness and parenchymal tissue volume. Septal wall thickness and numbers of open alveoli highly correlated with improved lung mechanics after SRT. In conclusion, reduction in surface tension was effective to stabilize alveoli linked with an attenuation of parameters of acute lung injury at D3 and collapse induration at D7. Hence, SRT modifies disease progression to collapse induration.

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