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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 (December 1, 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 of alveolar diameter provided a means for quantifying the time to complete liquid removal (C t ) in single alveoli. All determinations were obtained at an Pa of 5 cmH2O. C t , which related inversely to alveolar diameter, averaged 4.5 s in alveoli with the fastest liquid removal. Injections of dye-stained liquid revealed that the liquid flowed from the injected alveoli to adjacent air-filled alveoli. Lung hyperinflations instituted by cycling Pa between 5 and 15 cmH2O decreased C t by 50%. Chelation of intracellular Ca2+ prolonged C t and abolished the inflation-induced enhancement of liquid removal. We conclude that when liquid is injected in a few alveoli, it rapidly flows to adjacent air-filled alveoli. The removal mechanisms are dependent on alveolar size, inflation, and intracellular Ca2+. We speculate that removal of liquid from the alveolar surface is determined by the curvature and surface-active properties of the air-liquid interface.
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Nunn, John F. "Alveolar Air Equations." Anesthesiology 85, no. 4 (October 1, 1996): 940. http://dx.doi.org/10.1097/00000542-199610000-00035.
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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 (April 1, 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 filled with an electrolyte solution, and midway through each measurement some of the solution was injected into the alveolar lumen. Injecting the solution without amiloride did not alter the alveolar PD (-1.0 +/- 0.4 before and -1.1 +/- 0.5 after injection). The alveolar PD decreased to -0.1 +/- 0.2 mV after injecting the solution with 10(-5) M amiloride into the alveolar interior. These results support the hypothesis that alveolar epithelium in air-filled lungs actively absorbs sodium in vivo, which accounts for the majority of the transepithelial PD.
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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 (September 15, 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, Lederer DJ, Bhattacharya J. Am J Respir Cell Mol Biol 44: 34–39, 2011) that the presence of a liquid-filled alveolus protrudes into the neighboring air-filled alveolus with the shared septal strain amounting to a maximum value of 1.374 (corresponding to the maximum stress of 5.12 kPa) even at functional residual capacity; on the other hand, it further shows that the pattern of alveolar expansion appears heterogeneous or homogeneous, strongly depending on differences in air-liquid interface tension on alveolar segments. The proposed model is a preliminary step toward picturing a global topographical distribution of stress and strain on the scale of the lung as a whole to prevent ventilator-induced lung injury.
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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 (February 1, 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 existed from airway to alveolar liquid across the air-liquid interface. We attribute this finding, on the basis of the Laplace equation, to an air-liquid interface of constant radius in all the lobes. In fact, we calculated from the Laplace equation an air-liquid interface radius which equalled morphological estimates of alveolar radius. We conclude that in the steady state, alveoli that contained liquid have a constant radius of curvature of the air-liquid interface possibly because they are always completely liquid filled.
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Conhaim, R. L. "Airway level at which edema liquid enters the air space of isolated dog lungs." Journal of Applied Physiology 67, no. 6 (December 1, 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 lobe into three horizontal layers and prepared fluorescence-microscopic sections of each layer. In the most apical layers where alveolar flooding was minimal, 10.6 +/- 21.0% (SD) of alveolar ducts were either fluorescence filled or air filled and continuous with fluorescence-filled alveoli. In the same layers, 11.0 +/- 19.0% of respiratory bronchioles were similarly labeled. No terminal bronchioles in these layers were fluorescence labeled. This suggested that the fluorescent albumin entered the air space across the epithelium of respiratory bronchioles, alveolar ducts, or their associated alveoli. To simulate an alternative explanation, i.e., that fluorescence first entered central airways then flowed into peripheral air spaces, we prepared two additional lobes that we first partially inflated with fluorescent albumin then filled to capacity with air. This pushed the fluorescent solution along the airways into the lung periphery. In these lobes the ciliary lining of bronchi and terminal bronchioles was fluorescence coated. By comparison, cilia in fluorescence-perfused lobes were not coated. We conclude that alveolar flooding in hydrostatic pulmonary edema occurs across the epithelium of alveolar ducts, respiratory bronchioles, or their associated alveoli.(ABSTRACT TRUNCATED AT 250 WORDS)
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Ochs, Matthias, Jan Hegermann, Elena Lopez-Rodriguez, Sara Timm, Geraldine Nouailles, Jasmin Matuszak, Szandor Simmons, Martin Witzenrath, and Wolfgang M. Kuebler. "On Top of the Alveolar Epithelium: Surfactant and the Glycocalyx." International Journal of Molecular Sciences 21, no. 9 (April 27, 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 review what is known about this glycocalyx and how it can be visualized using electron microscopy. The application of colloidal thorium dioxide as a staining agent reveals differences in the staining pattern between type I and type II alveolar epithelial cells and shows close associations of the glycocalyx with intraalveolar surfactant subtypes such as tubular myelin. These morphological findings indicate that specific spatial interactions between components of the surfactant system and those of the alveolar epithelial glycocalyx exist which may contribute to the maintenance of alveolar homeostasis, in particular to alveolar micromechanics, to the functional integrity of the air-blood barrier, to the regulation of the thickness and viscosity of the alveolar lining layer, and to the defence against inhaled pathogens. Exploring the alveolar epithelial glycocalyx in conjunction with the surfactant system opens novel physiological perspectives of potential clinical relevance for future research.
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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 (May 2007): 3425–29. http://dx.doi.org/10.1021/ac062009a.
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Porzionato, Andrea, Diego Guidolin, Veronica Macchi, Gloria Sarasin, Davide Grisafi, Cinzia Tortorella, Arben Dedja, Patrizia Zaramella, and Raffaele De Caro. "Fractal analysis of alveolarization in hyperoxia-induced rat models of bronchopulmonary dysplasia." American Journal of Physiology-Lung Cellular and Molecular Physiology 310, no. 7 (April 1, 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 raised in ambient air for 2 wk; 2) rats exposed to 60% oxygen for 2 wk; 3) rats raised in normoxia for 6 wk; and 4) rats exposed to 60% hyperoxia for 2 wk and to room air for further 4 wk. Normoxic 6-wk rats showed increased D and decreased lacunarity with respect to normoxic 2-wk rats, together with changes in all stereological parameters except for mean alveolar volume. Hyperoxia-exposed 2-wk rats showed significant changes only in total number of alveoli, mean alveolar volume, and lacunarity with respect to equal-in-age normoxic rats. In the comparison between 6-wk rats, the hyperoxia-exposed group showed decreased D and increased lacunarity, together with changes in all stereological parameters except for septal thickness. Analysis of receiver operating characteristic curves showed a comparable discriminatory power of D, lacunarity, and total number of alveoli; Lmand mean alveolar volume were less discriminative. D and lacunarity did not show significant changes when different segmentation thresholds were applied, suggesting that the fractal approach may be fit to automatic image analysis.
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Denny, E., and R. C. Schroter. "The Mechanical Behavior of a Mammalian Lung Alveolar Duct Model." Journal of Biomechanical Engineering 117, no. 3 (August 1, 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 of the separate elastin and collagen fiber contributions are similar in form to the behavior of saline-filled lungs treated with either elastase or collagenase. A comparison with our earlier model, based upon a single alveolus, shows the duct to have a behavior closer to reported experimental data.
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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 (August 2002): 477–88. http://dx.doi.org/10.1016/s1052-3359(02)00018-2.
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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 (August 1, 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 with a reduction of total fibre volume density. The saline-filled lung distensibility (Ks) remained constant with alveolar dimensions and increased with decreasing total fibre volume density. The degree of geometric anisotropy between the duct lumen and alveoli was computed over pressure-volume cycles. To preserve broadly isotropic behavior, parenchyma with smaller alveolar airspace length dimensions required higher concentrations of fibres located in the duct and less in the septa in comparison with parenchyma of larger airspace dimensions.
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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 (February 14, 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). The primitive alveoli were lined largely by type-I pneumocytes and mature type-II pneumocytes. The type-I pneumocytes displayed an intimate contact with the endothelial cells of the blood capillaries forming the blood–air barrier (0.90 ± 0.03 µm in thickness). On the 3rd day, we observed intense septation and massive formation of new secondary septa giving the alveolar sac a crenate appearance. The mean thickness of the air–blood barrier decreased to reach 0.78 ± 0.14 µm. On the 7th day, the terminal bronchiole epithelium consisted of ciliated and non-ciliated cells. The non-ciliated cells could be identified as Clara cells and serous cells. New secondary septa were formed, meanwhile the inter-alveolar septa become much thinner and the air–blood barrier thickness was 0.66 ± 0.03 µm. On the 14th day, the terminal bronchiole expanded markedly and the pulmonary alveoli were thin-walled. Inter-alveolar septa become much thinner and single capillary layers were observed. In the 1st month, the secondary septa increased in length forming mature cup-shaped alveoli. In the 2nd month, the lung tissue grew massively to involve the terminal respiratory unit. In the 3rd month, the pulmonary parenchyma appeared morphologically mature. All inter-alveolar septa showed a single-capillary layer, and primordia of new septa were also observed. The thickness of the air–blood barrier was much thinner; 0.56 ± 0.16 µm. TUNEL assay after birth revealed that the apoptotic cells were abundant and distributed in the epithelium lining of the pulmonary alveoli and the interstitium of the thick interalveolar septa. On the 7th day, and onward, the incidence of apoptotic cells decreased markedly. This study concluded that the lung development included two phases: the first phase (from birth to the 14th days) corresponds to the period of bulk alveolarization and microvascular maturation. The second phase (from the 14th days to the full maturity) corresponds to the lung growth and late alveolarization.
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Maus, Ulrich, Susanne Herold, Heidrun Muth, Regina Maus, Leander Ermert, Monika Ermert, Norbert Weissmann, 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 (January 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 an alveolar influx of monocytes that were recovered by bronchoalveolar lavage and separated from PKH26-stained rAMs by flow cytometry. Alveolar recruited monocytes showed a blood monocytic phenotype as assessed by cell surface expression of F4/80, CD11a, CD11b, CD18, CD49d, and CD62L. In contrast, CD14 was markedly upregulated on alveolar recruited monocytes together with increased tumor necrosis factor-α message, discriminating this monocyte population from peripheral blood monocytes and rAMs. Thus monocytes recruited into the alveolar air space of mice in response to JE/MCP-1 keep phenotypic features of blood monocytes but upregulate CD14 and are “primed” for enhanced responsiveness to endotoxin with increased cytokine expression.
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Rühl, Nina, Elena Lopez-Rodriguez, Karolin Albert, Bradford J. Smith, Timothy E. Weaver, Matthias Ochs, and Lars Knudsen. "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 (August 30, 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. After one day of SP-B deficiency the volume of alveolar fluid V(alvfluid,par) as well as BAL protein and albumin levels were normal while the surface area of injured alveolar epithelium S(AEinjure,sep) was significantly increased. Alveoli and alveolar surface area could be recruited by increasing the air inflation pressure. Quasi-static pressure-volume loops were characterized by an increased hysteresis while the inspiratory capacity was reduced. After 3 days, an increase in V(alvfluid,par) as well as BAL protein and albumin levels were linked with a failure of both alveolar recruitment and airway pressure-dependent redistribution of alveolar fluid. Over time, V(alvfluid,par) increased exponentially with S(AEinjure,sep). In conclusion, high surface tension induces alveolar epithelial injury prior to edema formation. After passing a threshold, epithelial injury results in vascular leakage and exponential accumulation of alveolar fluid critically hampering alveolar recruitability.
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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 (February 12, 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 gives us better resolution and clearer images without losing any details when mapping the particle velocities. More detailed particle trajectories under multiple forces with different directions in an alveolus are presented. The effects of flow patterns, drag force, gravity and gravity directions are evaluated. By tracing the particle trajectories in the alveoli, we find that the drag force contributes to the reversible motion of particles. However, compared to drag force, the gravity is the decisive factor for particle deposition in the alveoli.
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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 (July 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 alveolar cells suggests that they may be the source of the surface-active film. The normal alveolar lining layer is not present in lungs of infants who die from profound atelectasis and hyaline membrane disease. Whether its absence is a failure of development or attributable to inactivation is not established.
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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 attached as partial spheroids to the bifurcating airway ducts, while breathing-related wall deformation was included to simulate actual alveolar expansion and contraction. Current model predictions confirm previous notions that the location of the alveoli greatly influences the alveolar flow pattern, with recirculating flow dominant in the proximal lung region. In the midalveolar lung generations, the intensity of the recirculating flow inside alveoli decreases while radial flow increases. In the distal alveolar region, the flow pattern is completely radial. The micron/submicron particle simulation results, employing the Euler–Lagrange modeling approach, indicate that deposition depends on the inhalation conditions and particle size. Specifically, the particle deposition rate in the alveolar region increases with higher inhalation tidal volume and particle diameter. Compared to previous acinar models, the present system takes into account the entire acinar region, including both partially alveolated respiratory bronchioles as well the fully alveolated distal airways and alveolar sacs. In addition, the alveolar expansion and contraction have been calculated based on physiological breathing conditions which make it easy to compare and validate model results with in vivo lung deposition measurements. Thus, the current work can be readily incorporated into human whole-lung airway models to simulate/predict the flow dynamics of toxic or therapeutic aerosols.
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Bastacky, J., C. Y. Lee, J. Goerke, H. Koushafar, D. Yager, L. Kenaga, T. P. Speed, Y. Chen, and J. A. Clements. "Alveolar lining layer is thin and continuous: low-temperature scanning electron microscopy of rat lung." Journal of Applied Physiology 79, no. 5 (November 1, 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 micron over relatively flat portions of the alveolar walls, 0.89 micron at the alveolar wall junctions, and 0.09 micron over the protruding features (9 rats, 20 walls, 16 junctions, and 146 areas), for an area-weighted average thickness of 0.2 micron. The alveolar lining layer appears continuous, submerging epithelial cell microvilli and intercellular junctional ridges; varies from a few nanometers to several micrometers in thickness, and serves to smooth the alveolar air-liquid interface in lungs inflated to zone 1 or 2 conditions.
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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 (April 1999): 190–92. http://dx.doi.org/10.1177/014107689909200408.
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Azzam, Zaher S., Yochai Adir, Lynn Welch, Jiwang Chen, Joseph Winaver, Phillip Factor, Norberto Krivoy, Aaron Hoffman, Jacob I. Sznajder, and Zaid Abassi. "Alveolar fluid reabsorption is increased in rats with compensated heart failure." American Journal of Physiology-Lung Cellular and Molecular Physiology 291, no. 5 (November 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-Dawley male rats. Seven days after the placement of the fistula, AFR was studied in the isolated perfused rat lung model. AFR in control rats was 0.49 ± 0.02 ml/h (all values are means ± SE) and increased by ∼40% (0.69 ± 0.03 ml/h) in rats with chronic CHF ( P < 0.001). The albumin flux from the pulmonary circulation into the air spaces did not increase in the experimental groups, indicating that lung permeability for large solutes was not increased. Na+-K+-ATPase activity and protein abundance at the plasma membrane of distal alveolar epithelial tissue were significantly increased in CHF rats compared with controls. These changes were associated with increased plasma norepinephrine levels in CHF rats compared with controls. We provide evidence that in a rat model of chronic compensated CHF, AFR is increased, possibly due to increased endogenous norepinephrine upregulating active sodium transport and protecting against alveolar flooding.
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Hlastala, Michael P., Frank L. Powell, and Joseph C. Anderson. "Airway exchange of highly soluble gases." Journal of Applied Physiology 114, no. 5 (March 1, 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 monomethyl ether) that have high water and blood solubility. The impact of solubility on the relative distribution of airway exchange was studied. We conclude that an increase in water solubility shifts the distribution of gas exchange toward the mouth. Of the four gases studied, ethanol had the greatest decrease in partial pressure from the alveolus to the mouth at end exhalation. Single exhalation breath tests are inappropriate for estimating alveolar levels of highly soluble gases, particularly for ethanol.
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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 alveolar macrophages—thus limiting the inflammatory response that, if unchecked, could threaten the essential respiratory function of the alveolus—while upregulating the cell's phagocytotic activity. Finally, we examine the role that inadequate or inappropriate PPAR-γresponses play in specific lung diseases.
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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 (May 1, 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 alveolar epithelium in vivo. Nocodazole increased the number of vesicles in the alveolar epithelium and capillary endothelium. Monensin increased vesicle density in the endothelium. These results suggested that the inhibitors disrupted microtubules or interrupted cellular membrane traffic in the lung. Both inhibitors decreased lung parenchymal uptake of immunoreactive human albumin from the air spaces. Monensin and nocodazole inhibited albumin uptake in cultured alveolar type II cells. Monensin increased the amount of 125I-labeled surfactant protein A associated with the lungs, compared with the quantity remaining in the air space 2 h after instillation. Although the drugs decreased alveolar epithelial protein uptake, they did not decrease alveolar clearance of 125I-labeled immunoglobulin G or 131I-labeled albumin in anesthetized rabbits. Thus monensin- and nocodazole-sensitive protein-uptake pathways do not account for most alveolar protein clearance when the distal air spaces are filled with a protein solution.
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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 (November 1, 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 imaging to identify ATP-releasing sites. With LL solution introduced into air spaces, brief inflation of such edematous lung (1 s, ∼20 cmH2O) induced transient (<30 s) ATP release in a limited number of air-inflated alveolar sacs during their recruitment/opening. Released ATP reached concentrations of ∼10−6 M, relevant for autocrine/paracrine signaling, but it remained spatially restricted to single alveolar sacs or their clusters. ATP release was stimulus dependent: prolonged (100 s) inflation evoked long-lasting ATP release that terminated upon alveoli deflation/derecruitment while cyclic inflation/suction produced cyclic ATP release. With LL introduced into blood vessels, inflation induced transient ATP release in many small patchlike areas the size of alveolar sacs. Findings suggest that inflation induces ATP release in both alveoli and the surrounding blood capillary network; the functional units of ATP release presumably consist of alveolar sacs or their clusters. Our study demonstrates the feasibility of real-time ATP release imaging in ex vivo lungs and provides the first direct evidence of inflation-induced ATP release in lung air spaces and in pulmonary blood capillaries, highlighting the importance of purinergic signaling in lung function.
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Garat, C., S. Rezaiguia, M. Meignan, M. P. D'Ortho, A. Harf, M. A. Matthay, and C. Jayr. "Alveolar endotoxin increases alveolar liquid clearance in rats." Journal of Applied Physiology 79, no. 6 (December 1, 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-labeled albumin (6 ml/kg into both lungs). Alveolar liquid clearance was significantly greater at 24 h (36 +/- 5%) and 40 h (38 +/- 7%) after endotoxin exposure than in saline-instilled controls (27 +/- 6%). Although there was an influx of neutrophils into the air space, there was no increase in lung epithelial permeability to protein at 24 or 40 h. Amiloride (2 x 10(-3) M), a sodium channel inhibitor, significantly reduced alveolar liquid clearance in the rats exposed to endotoxin. However, the increase in alveolar liquid clearance was not inhibited when propranolol (2 x 10(-5) M) was added to the 5% albumin solution. Thus exposure to alveolar endotoxin upregulates net alveolar fluid clearance in vivo for up to 40 h, a potentially important mechanism for accelerating alveolar fluid clearance under some pathological conditions. The increase in alveolar liquid clearance 24 and 40 h after instillation of endotoxin into the air spaces is mediated by an increased uptake of sodium through amiloride-sensitive sodium channels.
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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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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 (September 1997): 1191–95. http://dx.doi.org/10.1289/ehp.97105s51191.
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Farkas, Laszlo, Daniela Farkas, David Warburton, Jack Gauldie, Wei Shi, Martin R. Stampfli, Norbert F. Voelkel, and Martin Kolb. "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 (October 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 space enlargement, alveolar cell proliferation, and apoptosis. Furthermore, laser-capture microdissection and real-time PCR were used to measure compartment-specific gene expression. We then compared the effects of cigarette smoke exposure on Smad3−/− and littermate controls. Smad3 knockout resulted in the development of air space enlargement in the adult mouse and was associated with decreased alveolar VEGF levels and activity and increased alveolar cell apoptosis. Cigarette smoke exposure aggravated air space enlargement and alveolar cell apoptosis. We also found increased Smad2 protein expression and phosphorylation, which was enhanced following cigarette smoke exposure, in Smad3-knockout animals. Double immunofluorescence analysis revealed that endothelial apoptosis started before epithelial apoptosis. Our data indicate that balanced TGF-β signaling is not only important for regulation of extracellular matrix turnover, but also for alveolar cell homeostasis. Impaired signaling via the Smad3 pathway results in alveolar cell apoptosis and alveolar destruction, likely via increased Smad2 and reduced VEGF expression and might represent a predisposition for accelerated development of emphysema due to cigarette smoke exposure.
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Marzani, Andrieta Berliana, Angelica Rosa Septiana Hartono, Chris Monalisa, Cindy Thalia Putri, Jessica Natasya Caesaria, Kevin Axel Laurent Susanto, Novinka Iriane, et al. "Hyaline Membrane Disease in Preterm Newborn." Medical Clinical Update 1, no. 1 (October 17, 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, bell-shaped thorax, and air bronchograms. This case study showed chest x-ray finding of preterm newborn that diagnosed with respiratory distress syndrome clinically.
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Bachofen, H., S. Schurch, and F. Possmayer. "Disturbance of alveolar lining layer: effects on alveolar microstructure." Journal of Applied Physiology 76, no. 5 (May 1, 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 interfacial tension. In accordance, the alveolar microstructure and surface area of hexadecane-filled lungs resemble those of saline-filled lungs. 2) The P-V loops of fluorocarbon-filled lungs are not shifted to the left but coincide with those of fluorocarbon-rinsed lungs. Under both conditions, the alveolar microstructure is qualitatively identical and the alveolar surface areas are markedly reduced compared with normal air-filled lungs. These findings show that fluorocarbon-filled or fluorocarbon-rinsed lungs are subjected to similar interfacial tensions at the alveolar level. 3) Hexadecane-rinsed lungs show a pear-shaped P-V curve and a complex surface texture of peripheral air spaces. These results, together with in vitro observations, suggest a metamorphic interplay between lung surfactant and hexadecane in lining the surface and determining the surface tension. Evidently, the effects of foreign liquids introduced into the lung on the structure-function relationship cannot accurately be predicted from their in vitro surface tensions. This fact should be considered in the development of artificial surfactants.
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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 (April 1, 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 fibers was normal 12 wk after instillation of elastase, the volume of elastic fibers in alveolar entrance rings remained significantly reduced. In serial sections of elastic fibers, numerous gaps or separations in the normally continuous band of elastic fibers that encircle each alveolus were identified 1 wk after elastase instillation. There were 169 +/- 8 (SE), 62 +/- 32, and 12 +/- 6 gaps per millimeter of alveolar entrance ring circumference at 1, 4, and 12 wk, respectively, in the elastase-treated groups. The number of gaps at 12 wk was equivalent to two gaps or discontinuities in the elastic fibers of every alveolar entrance ring. No gaps or separations in elastic fibers were detected at 1, 4, or 12 wk in the control groups. These defects occur in concordance with the progression of air space enlargement and presumably contribute to the progression of air space enlargement that occurs after the elastin content of the tissue has returned to normal.
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Hyde, Dallas M., Shelley A. Blozis, Mark V. Avdalovic, Lei F. Putney, Rachel Dettorre, Nathanial J. Quesenberry, Paramjit Singh, and Nancy K. Tyler. "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 (September 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, and sectioned for alveolar counting. Parenchymal, alveolar, alveolar duct core air, and interalveolar septal tissue volumes increased rapidly during the first 2 yr with slowed growth from 2 to 7 yr. The rate of change was greater in males than females. Nalv also showed consistent growth throughout the study, with increases in Nalv best predicted by increases in lung volume. However, mean alveolar volume showed little relationship with age, lung volume, or body weight but was larger in females and showed a greater size distribution than in males. Alveoli increase in number but not volume throughout postnatal development in rhesus monkeys.
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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 (December 15, 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, pneumomediastinum, pneumopericardium, subcutaneous emphysema) suspected films reviewed by attending intensivist and radiologist. Results Of the 820 ill COVID-19 subjects in ICUs, 492(60%) were male, and 328 (40%) were female. The Mean age of 820 subjects was 60.84 + 16.82. 584 (71.22%) of subjects were non-intubated, and 236 (28.78%) were intubated. Alveolar air leak occurred in 98 (11.95%) of subjects. Alveolar air leak episodes include pneumothorax in 26 (3.17%), subcutaneous emphysema in 72 (8.78%), pneumomediastinum in 9 (1.10%), and pneumopericardium in 1 (0.12%) of subjects. The mean age in non-intubated subjects was 59.65 + 16.84, and for intubated subjects was 63 + 16.42. There was a significant difference in age between the groups who get intubated, versus not intubated P 0.001. Of the 584 non-intubated subjects, 31 (5.31%) had subcutaneous emphysema, of the 236 intubated subjects, 41 (17.37%) had subcutaneous emphysema. Difference between groups was statistically significant, P <0.001. When we compared intubated and non-intubated patients in case of total numbers of alveolar air leak episodes, the difference was statistically significant P <0.001. Conclusion According to this study, intubation was implemented more in older patients. Also, invasive ventilation was significantly associated with subcutaneous emphysema and total number of alveolar air leak episodes. In every patient with exaggeration of hypoxia, dyspnea or chest pain, pneumothorax should be kept in mind as a differential diagnosis. Keywords: COVID-19; Respiratory failure; Alveolar air leak; Paraseptal emphysema
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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 (August 31, 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 unique characteristics of the alveolar macrophage pool ontogeny, phenotypic heterogeneity and plasticity during homeostasis, tissue injury and normal ageing. We also discuss new evidence arising from recent studies where investigators described how the epigenetic landscape drives the specific gene expression profile of alveolar macrophages. Altogether, new analysis of macrophages by means of “omic” technologies will allow us to identify key pathways by which these cells contribute to the development and resolution of lung disease in both mice and humans.
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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 range of 0.3-1.1 micron or 3 mg latex beads with a particle size range of 0.3-0.6 micron, suspended in 1.0 ml 0.9% NaCl solution. Groups of 2-3 rats were killed by halothane overexposure at 5-180 minutes after instillation. The lungs were fixed in situ with McDowellTrumps. Lung tissue was embedded in plastic and stained-with uranyl acetate and lead citrate for electron microscopic examination.
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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 (April 1, 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 various types of lung injury. The model was used to predict Δ as a function of the inflation level (with the assumption of sequential alveolar recruitment, partly parallel to distension) and to simulate pulmonary edema by deriving equations that describe Δ for a collection of spherical shells representing combinations of collapsed, flooded, and inflated alveoli. Our theoretical data were compared with those provided by other models and with experimental data obtained from the literature. Our results suggest that NMR Δ measurements can be used to study the mechanisms underlying the lung pressure-volume behavior, to characterize lung injury, and to assess the contributions of alveolar recruitment and distension to the lung volume changes in response to the application of positive airway pressure (e.g., positive end-expiratory pressure).
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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 (December 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 the thoracic cavity (the thoracic cavity and lungs enlarge). Increasing the volume of the thoracic cavity reduces alveolar pressure below atmospheric pressure (barometric pressure), and air moves into the alveoli by bulk flow. In contrast, the impact of the organs against the diaphragm at each landing causes expiration. Specifically, upon landing, the abdominal organs flop into the diaphragm, causing it to return to its dome shape and decreasing the vertical dimension of the thoracic cavity. This compresses the alveolar gas volume and elevates alveolar pressure above barometric pressure, so air is expelled. To demonstrate this phenomenon, the plunger of a syringe model of the respiratory system was inserted through a compression spring. Holding the syringe and pressing the plunger firmly against a hard surface expels air from the lungs (the balloon within the syringe deflates) and compresses the spring. This models the kangaroo landing after a hop forward. Subsequently, the compression spring provides the energy for the “kangaroo” to “hop” forward upon the release of the syringe, and air enters the lungs (the balloon within the syringe inflates). The model accurately reflects how a hopping kangaroo breathes. A model was chosen to demonstrate this phenomenon because models engage and inspire students as well as significantly enhance student understanding.
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Conkin, Johnny. "Equivalent Air Altitude and the Alveolar Gas Equation." Aerospace Medicine and Human Performance 87, no. 1 (January 1, 2016): 61–64. http://dx.doi.org/10.3357/amhp.4421.2016.
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Singhal, Sunil, Victor A. Ferraris, Charles R. Bridges, Ellen R. Clough, John D. Mitchell, Hiran C. Fernando, and Joseph B. Shrager. "Management of Alveolar Air Leaks After Pulmonary Resection." Annals of Thoracic Surgery 89, no. 4 (April 2010): 1327–35. http://dx.doi.org/10.1016/j.athoracsur.2009.09.020.
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Cutillo, A. G., K. Ganesan, D. C. Ailion, A. H. Morris, C. H. Durney, S. C. Symko, and R. A. Christman. "Alveolar air-tissue interface and nuclear magnetic resonance behavior of lung." Journal of Applied Physiology 70, no. 5 (May 1, 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 pressures of 0-30 cmH2O for asymmetry times (a) of 1-6 ms. Delta was low in degassed lungs and increased markedly with alveolar opening when measured at a = 6 ms (delta 6 ms); delta 6 ms varied little during the rest of the inflation-deflation cycle. Delta 1 ms (a = 1 ms) did not vary significantly on inflation and deflation. Measurements of delta at a = 3 and 5 ms generally lay between those of delta 1 ms and delta 6 ms. These findings, which are consistent with theoretical predictions, suggest that measurements of delta at appropriate asymmetry times are particularly sensitive to alveolar opening and may provide a means of distinguishing alveolar recruitment from alveolar distension in the pressure-volume behavior of the lung.
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Porzionato, Andrea, Patrizia Zaramella, Arben Dedja, Diego Guidolin, Luca Bonadies, Veronica Macchi, Michela Pozzobon, 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 (May 1, 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 additional 4 weeks and treated with (b) IT-administered saline solution ( n = 10), or (c) MSC-EVs ( n = 10) on postnatal days 3, 7, 10, and 21. Hyperoxia exposure produced significant decreases in total number of alveoli, total surface area of alveolar air spaces, and proliferation index, together with increases in mean alveolar volume, mean linear intercept and fibrosis percentage; all these morphometric changes were prevented by MSC-EVs treatment. The medial thickness index for <100 µm vessels was higher for hyperoxia-exposed/sham-treated than for normoxia-exposed rats; MSC-EV treatment significantly reduced this index. There were no significant differences in interstitial/alveolar and perivascular F4/8-positive and CD86-positive macrophages. Conversely, hyperoxia exposure reduced CD163-positive macrophages both in interstitial/alveolar and perivascular populations and MSC-EV prevented these hyperoxia-induced reductions. These findings further support that IT-administered EVs could be an effective approach to prevent/treat BPD, ameliorating the impaired alveolarization and pulmonary artery remodeling also in a long-term model. M2 macrophage polarization could play a role through anti-inflammatory and proliferative mechanisms.
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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 (September 1, 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 HGF induces a remodeling within septal walls. Electroporation of a plasmid of human HGF gene controlled by the surfactant protein C promoter was applied for targeted gene transfer. Using design-based stereology at light and electron microscopic level, structural alterations were analyzed and compared with a control group. HGF gene transfer increased the volume of distal air spaces, as well as the surface area of the alveolar epithelium. The volume of septal walls, as well as the number of alveoli, was unchanged. Volumes per lung of collagen and elastic fibers were unaltered, but a marked reduction of the volume of residual extracellular matrix (all components other than collagen and elastic fibers) and interstitial cells was found. A correlation between the volumes of residual extracellular matrix and distal air spaces, as well as total surface area of alveolar epithelium, could be established. Cell-specific expression of HGF leads to a remodeling of the connective tissue within the septal walls in the healthy lung, which is associated with more pronounced stretching of distal air spaces at a given hydrostatic pressure during instillation fixation.
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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 (November 25, 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 analysis of inhaled air and exhaled breath, was developed and tested in 18 healthy individuals. For this, two BreathDiscovery instruments were coupled with each other.Measurements of inhaled air and exhaled breath in 18 healthy individuals (mean age 46±10.9 years; nine men, nine women) identified 35 different volatile organic compounds (VOCs) for further analysis. Not all of these had positive alveolar gradients and could be regarded as endogenous VOCs: 16 VOCs had a positive alveolar gradient in mean; 19 VOCs a negative one. 12 VOCs were positive in >12 of the healthy subjects.For the first time in our understanding, a method is described that enables simultaneous measurement of inhaled air and exhaled breath. This facilitates the calculation of alveolar gradients and selection of endogenous VOCs for exhaled breath analysis. Only a part of VOCs in exhaled breath are truly endogenous VOCs. The observation of different and varying polarities of the alveolar gradients needs further analysis.
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Batenburg, J. J. "Surfactant phospholipids: synthesis and storage." American Journal of Physiology-Lung Cellular and Molecular Physiology 262, no. 4 (April 1, 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 these cells serve as storage depot for the surfactant before this is secreted onto the alveolar surface. This article reviews the pathways via which the surfactant lipids are synthesized, our current knowledge of the regulation of these pathways, and what is known about intracellular traffic of phospholipids from their site of synthesis to the lamellar bodies.
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Maus, Ulrich a., M. Audrey Koay, Tim Delbeck, Matthias Mack, Monika Ermert, Leander Ermert, Timothy S. Blackwell, 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 (June 1, 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 affect the JE/MCP-1-driven alveolar monocyte accumulation, despite the observation that rAM constitutively expressed the JE/MCP-1 receptor CCR2, as analyzed by flow cytometry and immunohistochemistry. In contrast, depletion of rAM largely suppressed alveolar cytokine release as well as neutrophil and monocyte recruitment profiles upon combined JE/MCP-1/LPS treatment. Despite this strongly attenuated alveolar inflammatory response, increased lung permeability was still observed in rAM-depleted mice undergoing JE/MCP-1/LPS challenge. Lung leakage was abrogated by codepletion of circulating neutrophils or administration of anti-CD18. Collectively, rAM are not involved in JE/MCP-1-driven alveolar monocyte recruitment in noninflamed lungs but largely contribute to the alveolar cytokine response and enhanced early neutrophil and delayed monocyte influx under inflammatory conditions (JE/MCP-1/LPS deposition). Loss of lung barrier function observed under these conditions is rAM independent but involves circulating neutrophils via β2-integrin engagement.
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Wang, Yanjie, Zan Tang, Huanwei Huang, Jiao Li, Zheng Wang, Yuanyuan Yu, Chengwei Zhang, 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 (February 20, 2018): 2407–12. http://dx.doi.org/10.1073/pnas.1719474115.
Full textAbstract:
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 during alveologenesis and in post pneumonectomy (PNX) newly formed alveoli. We found that the adult AT1 cell population contains both Hopx+Igfbp2+ and Hopx+Igfbp2− AT1 cells, which have distinct cell fates during alveolar regeneration. Using an Igfbp2-CreER mouse model, we demonstrate that Hopx+Igfbp2+ AT1 cells represent terminally differentiated AT1 cells that are not able to transdifferentiate into AT2 cells during post-PNX alveolar regeneration. Our study provides tools and insights that will guide future investigations into the molecular and cellular mechanism or mechanisms underlying AT1 cell fate during lung development and regeneration.
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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 (January 1, 1991): 63–69. http://dx.doi.org/10.1152/jappl.1991.70.1.63.
Full textAbstract:
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 hyperpolarization, a response also noted for large airways. When the airways were blocked by an immiscible nonconducting fluorocarbon, basal PD was not different from unblocked lobes (4.0 mV) but was inhibited 73% by luminal amiloride. Cl(-)-free Krebs-Ringer-bicarbonate blocked in the alveoli with fluorocarbon did not induce hyperpolarization. This result suggests that 1) Cl- permselectivity of the alveolar epithelium is less than that of large airway epithelium and 2) airway PD dominates the voltage across the liquid-filled lung, even when measurements are made from alveoli. When airways are blocked by fluorocarbon, the PD across the alveolar epithelium is largely dependent on Na+ flow through a path with amiloride-sensitive channels.
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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 (August 1992): 740–41. http://dx.doi.org/10.1017/s0424820100124100.
Full textAbstract:
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 frozen specimen from the inflated lung. This requirement precludes the possibility of having a cryogen come into primary contact with the internal surface of an alveolus. However, if optimal fixation through the pleura could be attained, then the lining layers of subjacent alveoli could be studied. In this report, we describe a new method to cryopreserve distal lung tissue for optimal study of the extracellular lining layers of the alveolus. Alveolar tissue is sufficiently preserved in the inflated state to maintain its in vivo characteristics.
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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 (May 1, 1996): 1431–45. http://dx.doi.org/10.1152/jappl.1996.80.5.1431.
Full textAbstract:
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 contribution of these receptors requires further studies. Little is known about alveolar clearance of protein during pathological conditions; further studies are required to determine the roles of the different cell types in the lung for removal of protein from the alveolar spaces of the lung. Alveolar macrophages are likely to play an important role in the degradation and removal of insoluble protein from the distal air spaces after acute lung injury. In conclusion, the present data suggest that most proteins and peptides deposited on the epithelial surfaces in the distal air spaces are cleared as intact molecules, predominantly via paracellular routes. The contribution of pinocytic processes appear to be of minor importance for translocation of bulk quantities of proteins or peptides across the alveolar epithelium.