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Artículos de revistas sobre el tema "Alveolar air"

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Publicado: 11 de marzo de 2023

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1

Wang, P. M., Y. Ashino, H. Ichimura, and J. Bhattacharya. "Rapid alveolar liquid removal by a novel convective mechanism." American Journal of Physiology-Lung Cellular and Molecular Physiology 281, no. 6 (2001): L1327—L1334. http://dx.doi.org/10.1152/ajplung.2001.281.6.l1327.

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Although alveoli clear liquid by active transport, the presence of surface-active material on the alveolar surface suggests that convective mechanisms for rapid liquid removal may exist. To determine such mechanisms, we held the isolated blood-perfused rat lung at a constant alveolar pressure (Pa). Under videomicroscopy, we micropunctured a single alveolus to infuse saline or Ringer solution in ∼10 adjacent alveoli. Infused alveoli were lost from view. However, as the infused liquid cleared, the alveoli reappeared and their diameters could be quantified. Hence the time-dependent determination
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2

Nunn, John F. "Alveolar Air Equations." Anesthesiology 85, no. 4 (1996): 940. http://dx.doi.org/10.1097/00000542-199610000-00035.

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3

Nielson, D. W., and M. B. Lewis. "Effects of amiloride on alveolar epithelial PD and fluid composition in rabbits." American Journal of Physiology-Lung Cellular and Molecular Physiology 258, no. 4 (1990): L215—L219. http://dx.doi.org/10.1152/ajplung.1990.258.4.l215.

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To look for evidence of active absorption of Na+ in the alveolus in vivo in air-filled lungs, we measured [K+] and [Cl-] in the alveolar lining fluid and the potential difference (PD) across the alveolar epithelium by puncturing alveoli in lungs of anesthetized rabbits with nonselective and ion-selective microelectrodes. After intravenous doses of amiloride, the PD and [K+] decreased (-1.0 +/- 0.3 to -0.3 +/- 0.1 mV, 7.4 +/- 1.1 to 4.2 +/- 0.4 meq/l, P less than 0.001), but [Cl-] did not change (96 +/- 9, 94 +/- 4 meq/l). In another set of experiments, the PD was measured with microelectrodes
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4

Chen, Zheng-long, Ya-zhu Chen, and Zhao-yan Hu. "A micromechanical model for estimating alveolar wall strain in mechanically ventilated edematous lungs." Journal of Applied Physiology 117, no. 6 (2014): 586–92. http://dx.doi.org/10.1152/japplphysiol.00072.2014.

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To elucidate the micromechanics of pulmonary edema has been a significant medical concern, which is beneficial to better guide ventilator settings in clinical practice. In this paper, we present an adjoining two-alveoli model to quantitatively estimate strain and stress of alveolar walls in mechanically ventilated edematous lungs. The model takes into account the geometry of the alveolus, the effect of surface tension, the length-tension properties of parenchyma tissue, and the change in thickness of the alveolar wall. On the one hand, our model supports experimental findings (Perlman CE, Lede
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5

Raj, J. U., R. L. Conhaim, and J. Bhattacharya. "Micropuncture measurement of alveolar liquid pressure in excised dog lung lobes." Journal of Applied Physiology 62, no. 2 (1987): 781–84. http://dx.doi.org/10.1152/jappl.1987.62.2.781.

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We have investigated the mechanism of alveolar liquid filling in pulmonary edema. We excised, degassed, and intrabronchially filled 14 dog lung lobes from nine dogs with 75, 150, 225, or 350 ml of 5% albumin solution, and then air inflated the lobes to a constant airway pressure of 25 cmH2O. By use of micropipettes, we punctured subpleural alveoli to measure alveolar liquid pressure by the servo-null technique. Alveolar liquid pressure was constant in all lobes despite differences in lobe liquid volume and averaged 10.6 +/- 1.3 cmH2O. Thus, in all lobes a constant pressure drop of 14.4 cmH2O e
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6

Conhaim, R. L. "Airway level at which edema liquid enters the air space of isolated dog lungs." Journal of Applied Physiology 67, no. 6 (1989): 2234–42. http://dx.doi.org/10.1152/jappl.1989.67.6.2234.

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To identify lung units associated with liquid leakage into the air space in high-pressure pulmonary edema, we perfused air-inflated dog lung lobes with albumin solution to fill the loose peribronchovascular interstitium. Next, we perfused the lobes for 90 s with fluorescent albumin solution then froze the lobes in liquid nitrogen. This procedure confined the fluorescent perfusate to the liquid flux pathway between the circulation and the air space and eliminated the previously filled peribronchovascular cuffs as a source of the fluorescence that entered the air space. We divided each frozen lo
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7

Ochs, Matthias, Jan Hegermann, Elena Lopez-Rodriguez, et al. "On Top of the Alveolar Epithelium: Surfactant and the Glycocalyx." International Journal of Molecular Sciences 21, no. 9 (2020): 3075. http://dx.doi.org/10.3390/ijms21093075.

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Gas exchange in the lung takes place via the air-blood barrier in the septal walls of alveoli. The tissue elements that oxygen molecules have to cross are the alveolar epithelium, the interstitium and the capillary endothelium. The epithelium that lines the alveolar surface is covered by a thin and continuous liquid lining layer. Pulmonary surfactant acts at this air-liquid interface. By virtue of its biophysical and immunomodulatory functions, surfactant keeps alveoli open, dry and clean. What needs to be added to this picture is the glycocalyx of the alveolar epithelium. Here, we briefly rev
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8

van den Velde, Sandra, Marc Quirynen, Paul van Hee, and Daniel van Steenberghe. "Differences between Alveolar Air and Mouth Air." Analytical Chemistry 79, no. 9 (2007): 3425–29. http://dx.doi.org/10.1021/ac062009a.

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9

Porzionato, Andrea, Diego Guidolin, Veronica Macchi, et al. "Fractal analysis of alveolarization in hyperoxia-induced rat models of bronchopulmonary dysplasia." American Journal of Physiology-Lung Cellular and Molecular Physiology 310, no. 7 (2016): L680—L688. http://dx.doi.org/10.1152/ajplung.00231.2015.

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No papers are available about potentiality of fractal analysis in quantitative assessment of alveolarization in bronchopulmonary dysplasia (BPD). Thus, we here performed a comparative analysis between fractal [fractal dimension ( D) and lacunarity] and stereological [mean linear intercept ( Lm), total volume of alveolar air spaces, total number of alveoli, mean alveolar volume, total volume and surface area of alveolar septa, and mean alveolar septal thickness] parameters in experimental hyperoxia-induced models of BPD. At birth, rats were distributed between the following groups: 1) rats rais
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10

Denny, E., and R. C. Schroter. "The Mechanical Behavior of a Mammalian Lung Alveolar Duct Model." Journal of Biomechanical Engineering 117, no. 3 (1995): 254–61. http://dx.doi.org/10.1115/1.2794178.

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A model for the mechanical properties of an alveolar duct is analyzed using the finite element method. Its geometry comprises an assemblage of truncated octahedral alveoli surrounding a longitudinal air duct. The amounts and distributions of elastin and collagen fiber bundles, modeled by separate stress-strain laws, are based upon published data for dogs. The surface tension of the air-liquid interface is modeled using an area-dependent relationship. Pressure-volume curves are computed that compare well with experimental data for both saline-filled and air-filled lungs. Pressure-volume curves
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11

Loran, David B., Kenneth J. Woodside, Robert J. Cerfolio, and Joseph B. Zwischenberger. "Predictors of alveolar air leaks." Chest Surgery Clinics of North America 12, no. 3 (2002): 477–88. http://dx.doi.org/10.1016/s1052-3359(02)00018-2.

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12

Denny, E., and R. C. Schroter. "Relationships Between Alveolar Size and Fibre Distribution in a Mammalian Lung Alveolar Duct Model." Journal of Biomechanical Engineering 119, no. 3 (1997): 289–97. http://dx.doi.org/10.1115/1.2796093.

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A finite element model, comprising an assemblage of tetrakaidecahedra or truncated octahedra, is used to represent an alveolar duct unit. The dimensions of the elastin and collagen fibre bundles, and the surface tension properties of the air-liquid interfaces, are based on available published data. Changes to the computed static pressure-volume behavior with variation in alveolar dimensions and fibre volume densities are characterized using distensibility indices (K). The air-filled lung distensibility (Ka) decreased with a reduction in the alveolar airspace length dimensions and increased wit
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13

Mokhtar, Doaa M., Manal T. Hussein, Marwa M. Hussein, Enas A. Abd-Elhafez, and Gamal Kamel. "New Insight into the Development of the Respiratory Acini in Rabbits: Morphological, Electron Microscopic Studies, and TUNEL Assay." Microscopy and Microanalysis 25, no. 3 (2019): 769–85. http://dx.doi.org/10.1017/s1431927619000059.

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AbstractThis study investigated the histomorphological features of developing rabbit respiratory acini during the postnatal period. On the 1st day of postnatal life, the epithelium of terminal bronchiole consisted of clear cells which intercalated between few ciliated and abundant non-ciliated (Clara) cells. At this age, the rabbit lung was in the alveolar stage. The terminal bronchioles branched into several alveolar ducts, which opened into atria that communicated to alveolar sacs. All primary and secondary inter-alveolar septa were thick and showed a double-capillary network (immature septa
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14

Maus, Ulrich, Susanne Herold, Heidrun Muth, et al. "Monocytes recruited into the alveolar air space of mice show a monocytic phenotype but upregulate CD14." American Journal of Physiology-Lung Cellular and Molecular Physiology 280, no. 1 (2001): L58—L68. http://dx.doi.org/10.1152/ajplung.2001.280.1.l58.

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The evaluation of monocytes recruited into the alveolar space under both physiological and inflammatory conditions is hampered by difficulties in discriminating these cells from resident alveolar macrophages (rAMs). Using the intravenous injected fluorescent dye PKH26, which accumulated in rAMs without labeling blood leukocytes, we developed a technique that permits the identification, isolation, and functional analysis of monocytes recruited into lung alveoli of mice. Alveolar deposition of murine JE, the homologue of human monocyte chemoattractant protein (MCP)-1 (JE/MCP-1), in mice provoked
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15

Rühl, Nina, Elena Lopez-Rodriguez, Karolin Albert, et al. "Surfactant Protein B Deficiency Induced High Surface Tension: Relationship between Alveolar Micromechanics, Alveolar Fluid Properties and Alveolar Epithelial Cell Injury." International Journal of Molecular Sciences 20, no. 17 (2019): 4243. http://dx.doi.org/10.3390/ijms20174243.

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High surface tension at the alveolar air-liquid interface is a typical feature of acute and chronic lung injury. However, the manner in which high surface tension contributes to lung injury is not well understood. This study investigated the relationship between abnormal alveolar micromechanics, alveolar epithelial injury, intra-alveolar fluid properties and remodeling in the conditional surfactant protein B (SP-B) knockout mouse model. Measurements of pulmonary mechanics, broncho-alveolar lavage fluid (BAL), and design-based stereology were performed as a function of time of SP-B deficiency.
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16

Dong, Jun, Yan Qiu, Huimin Lv, Yue Yang, and Yonggang Zhu. "Investigation on Microparticle Transport and Deposition Mechanics in Rhythmically Expanding Alveolar Chip." Micromachines 12, no. 2 (2021): 184. http://dx.doi.org/10.3390/mi12020184.

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The transport and deposition of micro/nanoparticles in the lungs under respiration has an important impact on human health. Here, we presented a real-scale alveolar chip with movable alveolar walls based on the microfluidics to experimentally study particle transport in human lung alveoli under rhythmical respiratory. A new method of mixing particles in aqueous solution, instead of air, was proposed for visualization of particle transport in the alveoli. Our novel design can track the particle trajectories under different force conditions for multiple periods. The method proposed in this study
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17

Jobe, Alan H. "The Alveolar Lining Layer: A Review of Studies on Its Role in Pulmonary Mechanics and in the Pathogenesis of Atelectasis, by Mary Ellen Avery, MD, Pediatrics, 1962:30:324–330." Pediatrics 102, Supplement_1 (1998): 234–36. http://dx.doi.org/10.1542/peds.102.s1.234.

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The alveoli of the normal lung are lined by a substance that exerts surface tension at the air–liquid interface. In the expanded lung, the tension is high and operates to increase the elastic recoil of the lung. In the lung at low volumes, the surface tension becomes extremely low. This confers stability on the air spaces and thus prevents atelectasis. This lining layer is a lipoprotein film, which is not found where alveoli still are lined by cuboidal epithelium. Its appearance coincides with the appearance of alveolar lining cells. Electron microscopic evidence of secretory activity in alveo
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18

Kolanjiyil, Arun V., and Clement Kleinstreuer. "Modeling Airflow and Particle Deposition in a Human Acinar Region." Computational and Mathematical Methods in Medicine 2019 (January 14, 2019): 1–13. http://dx.doi.org/10.1155/2019/5952941.

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The alveolar region, encompassing millions of alveoli, is the most vital part of the lung. However, airflow behavior and particle deposition in that region are not fully understood because of the complex geometrical structure and intricate wall movement. Although recent investigations using 3D computer simulations have provided some valuable information, a realistic analysis of the air-particle dynamics in the acinar region is still lacking. So, to gain better physical insight, a physiologically inspired whole acinar model has been developed. Specifically, air sacs (i.e., alveoli) were attache
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19

Bastacky, J., C. Y. Lee, J. Goerke, et al. "Alveolar lining layer is thin and continuous: low-temperature scanning electron microscopy of rat lung." Journal of Applied Physiology 79, no. 5 (1995): 1615–28. http://dx.doi.org/10.1152/jappl.1995.79.5.1615.

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The low-temperature electron microscope, which preserves aqueous structures as solid water at liquid nitrogen temperature, was used to image the alveolar lining layer, including surfactant and its aqueous subphase, of air-filled lungs frozen in anesthetized rats at 15-cmH2O transpulmonary pressure. Lining layer thickness was measured on cross fractures of walls of the outermost subpleural alveoli that could be solidified with metal mirror cryofixation at rates sufficient to limit ice crystal growth to 10 nm and prevent appreciable water movement. The thickness of the liquid layer averaged 0.14
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20

Kanagasabay, Robin R., Philippa M. Lamb, Diana M. Tait, and Brendan P. Madden. "Local radiotherapy for alveolar air leak." Journal of the Royal Society of Medicine 92, no. 4 (1999): 190–92. http://dx.doi.org/10.1177/014107689909200408.

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21

Azzam, Zaher S., Yochai Adir, Lynn Welch, et al. "Alveolar fluid reabsorption is increased in rats with compensated heart failure." American Journal of Physiology-Lung Cellular and Molecular Physiology 291, no. 5 (2006): L1094—L1100. http://dx.doi.org/10.1152/ajplung.00180.2005.

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Alveolar fluid reabsorption (AFR) is important in keeping the air spaces free of edema. This process is accomplished via active transport of Na+ across the alveolo-capillary barrier mostly by apical Na+ channels and basolateral Na+-K+-ATPases. Recently, we have reported that acute elevation of left atrial pressures is associated with decreased AFR in isolated rat lungs. However, the effect of chronic elevation of pulmonary capillary pressure, such as seen in patients with congestive heart failure (CHF), on AFR is unknown. CHF was induced by creating an aorto-caval fistula (ACF) in Sprague-Dawl
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22

Hlastala, Michael P., Frank L. Powell, and Joseph C. Anderson. "Airway exchange of highly soluble gases." Journal of Applied Physiology 114, no. 5 (2013): 675–80. http://dx.doi.org/10.1152/japplphysiol.01291.2012.

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Highly blood soluble gases exchange with the bronchial circulation in the airways. On inhalation, air absorbs highly soluble gases from the airway mucosa and equilibrates with the blood before reaching the alveoli. Highly soluble gas partial pressure is identical throughout all alveoli. At the end of exhalation the partial pressure of a highly soluble gas decreases from the alveolar level in the terminal bronchioles to the end-exhaled partial pressure at the mouth. A mathematical model simulated the airway exchange of four gases (methyl isobutyl ketone, acetone, ethanol, and propylene glycol m
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23

Smith, Monica R., Theodore J. Standiford, and Raju C. Reddy. "PPARs in Alveolar Macrophage Biology." PPAR Research 2007 (2007): 1–12. http://dx.doi.org/10.1155/2007/23812.

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PPARs, most notably PPAR-γ, play a crucial role in regulating the activation of alveolar macrophages, which in turn occupy a pivotal place in the immune response to pathogens and particulates drawn in with inspired air. In this review, we describe the dual role of the alveolar macrophage as both a first-line defender through its phagocytotic activity and a regulator of the immune response. Depending on its state of activation, the alveolar macrophage may either enhance or suppress different aspects of immune function in the lung. We then review the role of PPAR-γand its ligands in deactivating
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24

Hastings, R. H., J. R. Wright, K. H. Albertine, R. Ciriales, and M. A. Matthay. "Effect of endocytosis inhibitors on alveolar clearance of albumin, immunoglobulin G, and SP-A in rabbits." American Journal of Physiology-Lung Cellular and Molecular Physiology 266, no. 5 (1994): L544—L552. http://dx.doi.org/10.1152/ajplung.1994.266.5.l544.

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Protein in the alveolar space may be cleared by endocytosis and degradation inside alveolar epithelial cells, by transcytosis across the alveolar epithelium, or by restricted diffusion through the epithelium. The relative contributions of these three pathways to clearance of large quantities of protein from the air spaces is not known. This study investigated the effects of monensin and nocodazole, agents which inhibit endocytosis in cell culture, on alveolar epithelial protein transport in anesthetized rabbits. There was evidence that monensin and nocodazole inhibited endocytosis by the alveo
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25

Furuya, Kishio, Ju Jing Tan, Francis Boudreault, Masahiro Sokabe, Yves Berthiaume, and Ryszard Grygorczyk. "Real-time imaging of inflation-induced ATP release in the ex vivo rat lung." American Journal of Physiology-Lung Cellular and Molecular Physiology 311, no. 5 (2016): L956—L969. http://dx.doi.org/10.1152/ajplung.00425.2015.

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Extracellular ATP and other nucleotides are important autocrine/paracrine mediators that regulate diverse processes critical for lung function, including mucociliary clearance, surfactant secretion, and local blood flow. Cellular ATP release is mechanosensitive; however, the impact of physical stimuli on ATP release during breathing has never been tested in intact lungs in real time and remains elusive. In this pilot study, we investigated inflation-induced ATP release in rat lungs ex vivo by real-time luciferin-luciferase (LL) bioluminescence imaging coupled with simultaneous infrared tissue
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26

Garat, C., S. Rezaiguia, M. Meignan, et al. "Alveolar endotoxin increases alveolar liquid clearance in rats." Journal of Applied Physiology 79, no. 6 (1995): 2021–28. http://dx.doi.org/10.1152/jappl.1995.79.6.2021.

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Under some pathological conditions, ion transport across alveolar epithelial cells is downregulated, whereas under other pathological conditions, it may be upregulated. Because endotoxin is a biologically relevant pathological stimulus, we investigated the effect of endotoxin on alveolar epithelial liquid clearance in vivo. Escherichia coli endotoxin (220 micrograms/kg) was instilled into the lungs via the trachea of rats. Then, 24 or 40 h after endotoxin instillation, alveolar and lung liquid clearances were studied over 1 h by instillation of a 5% albumin solution with 1.5 microCi of 125I-la
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27

Goldsmith, Carroll-Ann, Charles Frevert, Amy Imrich, Constantinos Sioutas, and Lester Kobzik. "Alveolar Macrophage Interaction with Air Pollution Particulates." Environmental Health Perspectives 105 (September 1997): 1191. http://dx.doi.org/10.2307/3433531.

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28

Goldsmith, C. A., C. Frevert, A. Imrich, C. Sioutas, and L. Kobzik. "Alveolar macrophage interaction with air pollution particulates." Environmental Health Perspectives 105, suppl 5 (1997): 1191–95. http://dx.doi.org/10.1289/ehp.97105s51191.

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29

Farkas, Laszlo, Daniela Farkas, David Warburton, et al. "Cigarette smoke exposure aggravates air space enlargement and alveolar cell apoptosis in Smad3 knockout mice." American Journal of Physiology-Lung Cellular and Molecular Physiology 301, no. 4 (2011): L391—L401. http://dx.doi.org/10.1152/ajplung.00369.2010.

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The concept of genetic susceptibility factors predisposing cigarette smokers to develop emphysema stems from the clinical observation that only a fraction of smokers develop clinically significant chronic obstructive pulmonary disease. We investigated whether Smad3 knockout mice, which develop spontaneous air space enlargement after birth because of a defect in transforming growth factor-β (TGF-β) signaling, develop enhanced alveolar cell apoptosis and air space enlargement following cigarette smoke exposure. We investigated Smad3−/− and Smad3+/+ mice at different adult ages and determined air
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30

Marzani, Andrieta Berliana, Angelica Rosa Septiana Hartono, Chris Monalisa, et al. "Hyaline Membrane Disease in Preterm Newborn." Medical Clinical Update 1, no. 1 (2022): 44–45. http://dx.doi.org/10.58376/mcu.v1i1.14.

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Hyaline membrane disease (HMD) is commonly found in preterm infants. This disease occurs as the result of surfactant deficiency due to prematurity. Surfactant deficiency results in increased alveolar surface tension, with resistance to inflation and alveolar collapse at the end of expiration. As a result, the alveoli are injured due to shear stresses on the alveolar walls. The injury could be seen in chest x-ray, as the most common radiological modality to help differentiate diagnosis. Plain chest x-ray findings of HMD are low lung volumes, diffuse, bilateral and symmetrical granular opacities
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31

Bachofen, H., S. Schurch, and F. Possmayer. "Disturbance of alveolar lining layer: effects on alveolar microstructure." Journal of Applied Physiology 76, no. 5 (1994): 1983–92. http://dx.doi.org/10.1152/jappl.1994.76.5.1983.

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To further study the influence of altered surface tensions on alveolar micromechanics, we analyzed the structure-function relationships in excised rabbit lungs filled with or rinsed by a fluorocarbon (approximately 15 mN/m) or by hexadecane (approximately 25 mN/m). The lungs were fixed and dehydrated by vascular perfusion, and the tissue samples were analyzed by light, transmission, and scanning electron microscopy. We made three observations. 1) Pressure-volume (P-V) loops hexadecane-filled lungs are shifted to the left and coincide with those of saline-filled lungs, indicating near-zero inte
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32

Mercer, R. R., and J. D. Crapo. "Structural changes in elastic fibers after pancreatic elastase administration in hamsters." Journal of Applied Physiology 72, no. 4 (1992): 1473–79. http://dx.doi.org/10.1152/jappl.1992.72.4.1473.

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Ultrastructural changes in lung parenchymal elastic fibers were studied morphometrically 1, 4, and 12 wk after a single 12-unit dose of pancreatic elastase and in a saline-instilled control group. The mean linear intercept of the parenchymal air spaces was increased in the 1-, 4-, and 12-wk post-elastase instillation groups compared with age-matched controls. The volume of alveolar connective tissue fibers predominantly composed of elastin (elastic fibers) was decreased by 35% 1 wk after the instillation of elastase but returned to control levels by 4 wk. Although the total volume of elastic f
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33

Hyde, Dallas M., Shelley A. Blozis, Mark V. Avdalovic, et al. "Alveoli increase in number but not size from birth to adulthood in rhesus monkeys." American Journal of Physiology-Lung Cellular and Molecular Physiology 293, no. 3 (2007): L570—L579. http://dx.doi.org/10.1152/ajplung.00467.2006.

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Postnatal developmental stages of lung parenchyma in rhesus monkeys is about one-third that of humans. Alveoli in humans are reported to be formed up to 8 yr of age. We used design-based stereological methods to estimate the number of alveoli ( Nalv) in male and female rhesus monkeys over the first 7 yr of life. Twenty-six rhesus monkeys (13 males ranging in age from 4 to 1,920 days and lung volumes from 41.7 to 602 cm3, 13 females ranging in age from 22 to 2,675 days and lung volumes from 43.5 to 380 cm3) were necropsied and lungs fixed, isotropically oriented, fractionated, sampled, embedded
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34

Najafi, Atabak, Farahnaz Fallahian, Arezoo Ahmadi, and Khadijeh Bakhtavar. "Alveolar air leak and paraseptal emphysema in severe COVID-19 disease." Journal of Mechanical Ventilation 2, no. 4 (2021): 114–23. http://dx.doi.org/10.53097/jmv.10034.

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Background Corona virus 2019 (COVID-19) pandemic spread in the world as a great medical crisis. Its pathophysiology, manifestations, complications, and management are not completely defined, yet. In this study frequency of alveolar air leak in critically ill COVID-19 subjects is explored. Methods A total of 820 critically ill COVID-19 subjects who admitted with respiratory insufficiency to ICUs of Sina University Hospital from March 2020 to June 2021 were included. All their chest x ray (CXR) and Computed tomography (CT) of chest were reviewed. All alveolar air leak episodes (pneumothorax, pne
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35

Morales-Nebreda, Luisa, Alexander V. Misharin, Harris Perlman, and G. R. Scott Budinger. "The heterogeneity of lung macrophages in the susceptibility to disease." European Respiratory Review 24, no. 137 (2015): 505–9. http://dx.doi.org/10.1183/16000617.0031-2015.

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Alveolar macrophages are specialised resident phagocytes in the alveolus, constituting the first line of immune cellular defence in the lung. As the lung microenvironment is challenged and remodelled by inhaled pathogens and air particles, so is the alveolar macrophage pool altered by signals that maintain and/or replace its composition. The signals that induce the recruitment of circulating monocytes to the injured lung, as well as their distinct gene expression profile and susceptibility to epigenetic reprogramming by the local environment remain unclear. In this review, we summarise the uni
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36

Sanders, C. L., K. E. McDonald, R. R. Adee, and K. E. Lauhala. "Phagocytosis of pulmonary deposited particles by Type 1 alveolar epithelium." Proceedings, annual meeting, Electron Microscopy Society of America 47 (August 6, 1989): 922–23. http://dx.doi.org/10.1017/s0424820100156596.

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The role of the alveolar epithelium in removal of deposited particles from the alveolar air space has not been well defined. Type II cells, although in close proximity to particles, do not participate in the phagocytosis of particles. How ever, a variety of alveolarly deposited particulates are phagocytized by type I cells. The rapid and efficient phagocytosis of particles in the air space by macrophages minimizes particle entry into more fixed tissues of the lung.Female, Wistar, young adult rats were given a single intratracheal instillation of either 25 mg iron oxide with a particle size ran
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37

Durney, Carl H., Antonio G. Cutillo, and David C. Ailion. "Magnetic resonance behavior of normal and diseased lungs: spherical shell model simulations." Journal of Applied Physiology 88, no. 4 (2000): 1155–66. http://dx.doi.org/10.1152/jappl.2000.88.4.1155.

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The alveolar air-tissue interface affects the lung NMR signal, because it results in a susceptibility-induced magnetic field inhomogeneity. The air-tissue interface effect can be detected and quantified by measuring the difference signal (Δ) from a pair of NMR images obtained using temporally symmetric and asymmetric spin-echo sequences. The present study describes a multicompartment alveolar model (consisting of a collection of noninteracting spherical water shells) that simulates the behavior of Δ as a function of the level of lung inflation and can be used to predict the NMR response to var
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38

Giuliodori, Mauricio J., Heidi L. Lujan, Hussein Janbaih, and Stephen E. DiCarlo. "How does a hopping kangaroo breathe?" Advances in Physiology Education 34, no. 4 (2010): 228–32. http://dx.doi.org/10.1152/advan.00050.2010.

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We developed a model to demonstrate how a hopping kangaroo breathes. Interestingly, a kangaroo uses less energy to breathe while hopping than while standing still. This occurs, in part, because rather than using muscle power to move air into and out of the lungs, air is pulled into (inspiration) and pushed out of (expiration) the lungs as the abdominal organs “flop” within the kangaroo's body. Specifically, as the kangaroo hops upward, the abdominal organs lag behind, and the insertion of the diaphragm is pulled toward its origin, flattening the dome and increasing the vertical dimension of th
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39

Conkin, Johnny. "Equivalent Air Altitude and the Alveolar Gas Equation." Aerospace Medicine and Human Performance 87, no. 1 (2016): 61–64. http://dx.doi.org/10.3357/amhp.4421.2016.

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40

Singhal, Sunil, Victor A. Ferraris, Charles R. Bridges, et al. "Management of Alveolar Air Leaks After Pulmonary Resection." Annals of Thoracic Surgery 89, no. 4 (2010): 1327–35. http://dx.doi.org/10.1016/j.athoracsur.2009.09.020.

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41

Cutillo, A. G., K. Ganesan, D. C. Ailion, et al. "Alveolar air-tissue interface and nuclear magnetic resonance behavior of lung." Journal of Applied Physiology 70, no. 5 (1991): 2145–54. http://dx.doi.org/10.1152/jappl.1991.70.5.2145.

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Inflated lungs are characterized by a short nuclear magnetic resonance (NMR) free induction decay (rapid disappearance of NMR signal), likely due to internal (tissue-induced) magnetic field inhomogeneity produced by the alveolar air-tissue interface. This phenomenon can also be detected using temporally symmetric and asymmetric NMR spin-echo sequences; these sequences generate a pair of NMR images from which a difference signal (delta) is obtained (reflecting the signal from lung water experiencing the air-tissue interface effect). We measured delta in normal excised rat lungs at inflation pre
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42

Porzionato, Andrea, Patrizia Zaramella, Arben Dedja, et al. "Intratracheal administration of mesenchymal stem cell-derived extracellular vesicles reduces lung injuries in a chronic rat model of bronchopulmonary dysplasia." American Journal of Physiology-Lung Cellular and Molecular Physiology 320, no. 5 (2021): L688—L704. http://dx.doi.org/10.1152/ajplung.00148.2020.

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Early therapeutic effect of intratracheally (IT)-administered extracellular vesicles secreted by mesenchymal stem cells (MSC-EVs) has been demonstrated in a rat model of bronchopulmonary dysplasia (BPD) involving hyperoxia exposure in the first 2 postnatal weeks. The aim of this study was to evaluate the protective effects of IT-administered MSC-EVs in the long term. EVs were produced from MSCs following GMP standards. At birth, rats were distributed in three groups: (a) animals raised in ambient air for 6 weeks ( n = 10); and animals exposed to 60% hyperoxia for 2 weeks and to room air for ad
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43

Leuenberger, Alexandra, Amiq Gazdhar, Gudrun Herrmann, Matthias Ochs, Thomas Geiser, and Lars Knudsen. "Cell-specific expression of human HGF by alveolar type II cells induces remodeling of septal wall tissue in the lung: a morphometric study." Journal of Applied Physiology 113, no. 5 (2012): 799–807. http://dx.doi.org/10.1152/japplphysiol.00411.2012.

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Hepatocyte growth factor (HGF) is involved in development and regeneration of the lungs. Human HGF, which was expressed specifically by alveolar epithelial type II cells after gene transfer, attenuated the bleomycin-induced pulmonary fibrosis in an animal model. As there are also regions that appear morphologically unaffected in fibrosis, the effects of this gene transfer to normal lungs is of interest. In vitro studies showed that HGF inhibits the formation of the basal lamina by cultured alveolar epithelial cells. Thus we hypothesized that, in the healthy lung, cell-specific expression of HG
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44

Westhoff, Michael, Maren Friedrich, and Jörg I. Baumbach. "Simultaneous measurement of inhaled air and exhaled breath by double multicapillary column ion-mobility spectrometry, a new method for breath analysis: results of a feasibility study." ERJ Open Research 8, no. 1 (2021): 00493–2021. http://dx.doi.org/10.1183/23120541.00493-2021.

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The high sensitivity of the methods applied in breath analysis entails a high risk of detecting analytes that do not derive from endogenous production. Consequentially, it appears useful to have knowledge about the composition of inhaled air and to include alveolar gradients into interpretation.The current study aimed to standardise sampling procedures in breath analysis, especially with multicapillary column ion-mobility spectrometry (MCC-IMS), by applying a simultaneous registration of inhaled air and exhaled breath.A “double MCC-IMS” device, which for the first time allows simultaneous anal
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45

Batenburg, J. J. "Surfactant phospholipids: synthesis and storage." American Journal of Physiology-Lung Cellular and Molecular Physiology 262, no. 4 (1992): L367—L385. http://dx.doi.org/10.1152/ajplung.1992.262.4.l367.

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Pulmonary surfactant, a complex consisting of 90% lipids and 10% specific proteins, lines the alveoli of the lung and prevents alveolar collapse and transudation by lowering the surface tension at the air-liquid interface. Dipalmitoylphosphatidylcholine constitutes approximately 50% of the surfactant lipids and is primarily responsible for the surface tension-lowering property of the surfactant mixture. This phospholipid, together with the other surfactant phospholipids, is produced at the endoplasmic reticulum of the alveolar type II epithelial cells. The characteristic lamellar bodies in the
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46

Maus, Ulrich a., M. Audrey Koay, Tim Delbeck, et al. "Role of resident alveolar macrophages in leukocyte traffic into the alveolar air space of intact mice." American Journal of Physiology-Lung Cellular and Molecular Physiology 282, no. 6 (2002): L1245—L1252. http://dx.doi.org/10.1152/ajplung.00453.2001.

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Intratracheal instillation of the monocyte chemoattractant JE/monocyte chemoattractant protein (MCP)-1 in mice was recently shown to cause increased alveolar monocyte accumulation in the absence of lung inflammation, whereas combined JE/MCP-1/lipopolysaccharide (LPS) challenge provoked acute lung inflammation with early alveolar neutrophil and delayed alveolar monocyte influx. We evaluated the role of resident alveolar macrophages (rAM) in these leukocyte recruitment events and related phenomena of lung inflammation. Depletion of rAM by pretreatment of mice with liposomal clodronate did not af
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47

Wang, Yanjie, Zan Tang, Huanwei Huang, et al. "Pulmonary alveolar type I cell population consists of two distinct subtypes that differ in cell fate." Proceedings of the National Academy of Sciences 115, no. 10 (2018): 2407–12. http://dx.doi.org/10.1073/pnas.1719474115.

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Pulmonary alveolar type I (AT1) cells cover more than 95% of alveolar surface and are essential for the air–blood barrier function of lungs. AT1 cells have been shown to retain developmental plasticity during alveolar regeneration. However, the development and heterogeneity of AT1 cells remain largely unknown. Here, we conducted a single-cell RNA-seq analysis to characterize postnatal AT1 cell development and identified insulin-like growth factor-binding protein 2 (Igfbp2) as a genetic marker specifically expressed in postnatal AT1 cells. The portion of AT1 cells expressing Igfbp2 increases du
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48

Ballard, S. T., and J. T. Gatzy. "Alveolar transepithelial potential difference and ion transport in adult rat lung." Journal of Applied Physiology 70, no. 1 (1991): 63–69. http://dx.doi.org/10.1152/jappl.1991.70.1.63.

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The complex morphology of the mammalian lung complicates characterization of solute transport across the intact alveolar epithelium. We impaled the subpleural alveolar epithelium with microelectrodes and measured the transepithelial potential difference (PD) of the liquid-filled vascular-perfused left lobe of the rat lung. When the air space was filled entirely with Krebs-Ringer-bicarbonate, the PD was 4.7 mV (lumen negative). The PD was not affected significantly by agents that modify either Na+ or Cl- transport, but replacement of luminal Cl- with gluconate resulted in a fourfold hyperpolari
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49

Godleski, John J., Rebecca C. Stearns, Marshall Katler, Robyn Rufner, Theresa D. Sweeney, and Fred G. Lightfoot. "In situ cryofixation of lung tissue using the PS1000, a hand-held metal mirror cryofixation device." Proceedings, annual meeting, Electron Microscopy Society of America 50, no. 1 (1992): 740–41. http://dx.doi.org/10.1017/s0424820100124100.

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We have previously reported methods to cryofix the extracellular lining layers of the large airways and trachea. We seek to study the extracellular lining layers of both airways and alveoli in situ because it is the interaction of these lining materials with inhaled particles that determines the subsequent responses of phagocytic cells to the particles. Cryopreservation of the lining fluids of lung parenchyma is difficult because of the complexity of distal lung structure, and the need to fix the lung in its natural state, i.e., filled with air. Any method used must be able to obtain the froze
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50

Folkesson, H. G., M. A. Matthay, B. R. Westrom, K. J. Kim, B. W. Karlsson, and R. H. Hastings. "Alveolar epithelial clearance of protein." Journal of Applied Physiology 80, no. 5 (1996): 1431–45. http://dx.doi.org/10.1152/jappl.1996.80.5.1431.

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Substantial progress has been made in understanding the rate, the pathways, and the mechanisms regulating alveolar protein removal from the uninjured lung. Whole animal studies and cellular studies have demonstrated that the majority of alveolar epithelial protein clearance occurs by passive nondegradative diffusional pathways. Some evidence, however, has been recently presented that alveolar epithelial cells express an albumin-binding receptor as well as a polymeric immunoglobulin receptor, both of which might be important for alveolar epithelial clearance of protein. However, the contributio
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