Volume dependence of airway and tissue  impedances in mice

Sly, Peter D.; Collins, Rachel A.; Thamrin, Cindy; Turner, Debra J.; Hantos, Zoltán

doi:10.1152/japplphysiol.00596.2002

Cited by 105 publications

(109 citation statements)

References 21 publications

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“…Hy values were measured for a V T of 2 ml and were also similar to those previously reported (36,38), which range from 2 to 3 cmH 2 O/ml, however, for smaller V T . We hence confirm that healthy mice lungs exhibit hysteretic behavior.…”

Section: Discussionsupporting

confidence: 88%

The olfactory system is affected by steroid aerosol treatment in mice

Mucignat‐Caretta¹,

Bondı̀²,

Rubini³

et al. 2009

American Journal of Physiology-Lung Cellular and Molecular Phys

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Asthma needs continuous treatment often for years. In humans, some drugs are administered via aerosol, therefore they come in contact with both respiratory and olfactory mucosa. We explored the possibility that antiasthma corticosteroid treatment could influence the olfactory function by passage through the nose. A group of mice was exposed twice daily for 42 days to fluticasone propionate aerosol and was compared with a control group. Olfactory behavior, respiratory mechanics, histology, and immunoreactivity in the olfactory system were assessed. Fluticasone-treated mice were slower in retrieving a piece of hidden food, but both groups were similarly fast when the food was visible. When a clearly detectable odor was present in the environment, all mice behaved in a similar way. Respiratory mechanics indices were similar in all mice except for the viscose resistance, which was reduced in fluticasone-treated mice. Olfactory mucosa of fluticasone-treated mice was thicker than that of controls. Slight but consistent differences in staining were present for Olfactory Marker Protein but not for other proteins. A mild impairment of olfactory function is present in mice chronically treated with fluticasone aerosol, apparently accompanied by slight modifications of the olfactory receptor cells, and suggests monitoring of olfactory function modifications in long-term steroid users.corticosteroid; behavior THE OLFACTORY SYSTEM IS CHARACTERIZED by a rapid turnover of receptor neurons, for which lifespan is ϳ1 mo, and a neuron turnover in the first relay station, the olfactory bulb (OB). The receptor axons make synapses with dendrites of mitral cells in the glomeruli (11). OB interneurons are continuously renewed by cells that differentiate from neural stem cells residing in the subventricular zone. They arrive into the OB via the rostral migratory stream and are subsequently integrated in OB circuits (25, 33). Other chemosensory organs are present in the nasal cavity, concurring to chemosensory perception (8,39). This dynamic network is sensitive to environmental challenges, which often result in mucosal damage that is subsequently reflected in OB, affecting olfactory sensitivity (9, 29).Pathological conditions of the airways may affect the olfactory performance. Both upper and lower airways diseases, for example allergic rhinitis and asthma, are treated with topical administration of corticosteroids. Fluticasone propionate (FP) is one of the most popular and safe treatments for both conditions (2) due to its hepatic metabolism that allows only a topic anti-inflammatory effect without adrenal suppression (31). Whereas the improvement in the pathological state is well-documented (in humans, see, for example, Refs. 13,24,30,34,37; in mice, Refs. 12,32), little is known about its possible effect on olfactory cells and in the subsequent olfactory performance.Corticosteroid inhalatory treatments are often long-lasting, therefore they may influence the quality of life of patients even if they induce only slight side effect. Inha...

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Section: Discussionsupporting

confidence: 88%

The olfactory system is affected by steroid aerosol treatment in mice

Mucignat‐Caretta¹,

Bondı̀²,

Rubini³

et al. 2009

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…Airway resistance decreases while tissue resistance increases with increasing lung volume and hence the partitioning of R rs to airway and tissue components may be more advantageous at a higher lung volume (29). We demonstrated similar marked partitioning of airway and tissue compartments in the preterm lamb when measurements were made at a positive end-expiratory pressure of 0.3 kPa (21), suggesting that similar findings are obtained in the low volume lung.…”

Section: Lung Function In Unsedated Newbornssupporting

confidence: 63%

“…The apparent negative correlation between tissue hysteresivity and length within this small and young infant cohort suggests that there may also be a change in the balance between viscous and elastic mechanical forces within the tissues during this alveolarization period of human lung development. Furthermore, hysteresivity would be expected to decrease with increasing lung volume, as collagen increasingly dominates lung mechanics with increasing lung volume (16,29,30). For the same reason, a reduction in hysteresivity with increasing body length is consistent with a maturational increase in the microscopic collagen content of the tissue.…”

Section: Lung Function In Unsedated Newbornsmentioning

confidence: 94%

Partitioning of Airway and Parenchymal Mechanics in Unsedated Newborn Infants

Pillow

Stocks²,

Sly

et al. 2005

Pediatr Res

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“…Second, relative to the life span of the mouse, the time course of the development of emphysema in mice is much faster than that in humans. Third, the chest wall plays a different role in mice than in humans, because the chest wall tissues are very soft in the former (16,30). The latter is an advantage, however, as it allows us to use respiratory mechanics as a surrogate for lung mechanics, which obviates the need for the unphysiological open-chest condition.…”

Section: Discussionmentioning

confidence: 99%

Structure–Function Relations in an Elastase-Induced Mouse Model of Emphysema

Hamakawa

Bartolák‐Suki

Parameswaran

et al. 2011

Am J Respir Cell Mol Biol

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Emphysema is a progressive disease characterized by the destruction of peripheral airspaces and subsequent decline in lung function. However, the relation between structure and function during disease progression is not well understood. The objective of this study was to assess the time course of the structural, mechanical, and remodeling properties of the lung in mice after elastolytic injury. At 2, 7, and 21 days after treatment with porcine pancreatic elastase, respiratory impedance, the constituents of lung extracellular matrix, and histological sections of the lung were evaluated. In the control group, no changes were observed in the structural or functional properties, whereas, in the treatment group, the respiratory compliance and its variability significantly increased by Day 21 (P , 0.001), and the difference in parameters decreased with increasing positive end-expiratory pressure. The heterogeneity of airspace structure gradually increased over time. Conversely, the relative amounts of elastin and type I collagen exhibited a peak (P , 0.01) at Day 2, but returned to baseline levels by Day 21. Structure-function relations manifested themselves in strong correlations between compliance parameters and both mean size and heterogeneity of airspace structure (r 2 . 0.9). Similar relations were also obtained in a network model of the parenchyma in which destruction was based on the notion that mechanical forces contribute to alveolar wall rupture. We conclude that, in a mouse model of emphysema, progressive decline in lung function is sensitive to the development of airspace heterogeneity governed by local, mechanical, forceinduced failure of remodeled collagen.

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Volume dependence of airway and tissue impedances in mice

Cited by 105 publications

References 21 publications

The olfactory system is affected by steroid aerosol treatment in mice

The olfactory system is affected by steroid aerosol treatment in mice

Partitioning of Airway and Parenchymal Mechanics in Unsedated Newborn Infants

Structure–Function Relations in an Elastase-Induced Mouse Model of Emphysema

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