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Journal articles on the topic 'Alveolar mechanics'

Author: Grafiati

Published: 4 June 2021

Last updated: 19 February 2022

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1

Prange, Henry D. "LAPLACE’S LAW AND THE ALVEOLUS: A MISCONCEPTION OF ANATOMY AND A MISAPPLICATION OF PHYSICS." Advances in Physiology Education 27, no. 1 (March 2003): 34–40. http://dx.doi.org/10.1152/advan.00024.2002.

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Both the anatomy and the mechanics of inflation of the alveoli, as presented in most textbooks of physiology, have been misunderstood and misrepresented. The typical representation of the acinus as a “bunch of grapes” bears no resemblance to its real anatomy; the alveoli are not independent little balloons. Because of the prevalence of this misconception, Laplace’s law, as it applies to spheres, has been invoked as a mechanical model for the forces of alveolar inflation and as an explanation for the necessity of pulmonary surfactant in the alveolus. Alveoli are prismatic or polygonal in shape,

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2

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

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3

Bates, Jason H. T. "Understanding Alveolar Mechanics." Critical Care Medicine 41, no. 5 (May 2013): 1374–75. http://dx.doi.org/10.1097/ccm.0b013e31827c02b8.

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4

LIU, TIANYA, YUXING WANG, XIAOYU LIU, LAN YUAN, DEYU LI, HUITING QIAO, and YUBO FAN. "EFFECTS OF ALVEOLAR MORPHOLOGY ON ALVEOLAR MECHANICS: AN EXPERIMENTAL STUDY OF MOUSE LUNG BASED ON TWO- AND THREE-DIMENSIONAL IMAGING METHODS." Journal of Mechanics in Medicine and Biology 19, no. 04 (June 2019): 1950027. http://dx.doi.org/10.1142/s0219519419500271.

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Understanding alveolar mechanics is important for preventing the possible lung injuries during mechanical ventilation. Alveolar clusters with smaller size are found having lower compliance in two-dimensional studies. But the influence of alveolar shape on compliance is unclear. In order to investigate how alveolar morphology affects their behavior, we tracked subpleural alveoli of isolated mouse lungs during quasi-static ventilation using two- and three-dimensional imaging techniques. Results showed that alveolar clusters with smaller size and more spherical shape had lower compliance. There w

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5

Sera, Toshihiro, Hideo Yokota, Gaku Tanaka, Kentaro Uesugi, Naoto Yagi, and Robert C. Schroter. "Murine pulmonary acinar mechanics during quasi-static inflation using synchrotron refraction-enhanced computed tomography." Journal of Applied Physiology 115, no. 2 (July 15, 2013): 219–28. http://dx.doi.org/10.1152/japplphysiol.01105.2012.

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We visualized pulmonary acini in the core regions of the mouse lung in situ using synchrotron refraction-enhanced computed tomography (CT) and evaluated their kinematics during quasi-static inflation. This CT system (with a cube voxel of 2.8 μm) allows excellent visualization of not just the conducting airways, but also the alveolar ducts and sacs, and tracking of the acinar shape and its deformation during inflation. The kinematics of individual alveoli and alveolar clusters with a group of terminal alveoli is influenced not only by the connecting alveolar duct and alveoli, but also by the ne

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6

Roan, Esra, and Christopher M. Waters. "What do we know about mechanical strain in lung alveoli?" American Journal of Physiology-Lung Cellular and Molecular Physiology 301, no. 5 (November 2011): L625—L635. http://dx.doi.org/10.1152/ajplung.00105.2011.

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The pulmonary alveolus, terminal gas-exchange unit of the lung, is composed of alveolar epithelial and endothelial cells separated by a thin basement membrane and interstitial space. These cells participate in the maintenance of a delicate system regulated not only by biological factors but also by the mechanical environment of the lung, which undergoes dynamic deformation during breathing. Clinical and animal studies as well as cell culture studies point toward a strong influence of mechanical forces on lung cells and tissues including effects on growth and repair, surfactant release, injury,

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7

Perlman, Carrie E. "On modeling edematous alveolar mechanics." Journal of Applied Physiology 117, no. 8 (October 15, 2014): 937. http://dx.doi.org/10.1152/japplphysiol.00696.2014.

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8

Wilson, Theodore A., Ron C. Anafi, and Rolf D. Hubmayr. "Mechanics of edematous lungs." Journal of Applied Physiology 90, no. 6 (June 1, 2001): 2088–93. http://dx.doi.org/10.1152/jappl.2001.90.6.2088.

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Using the parenchymal marker technique, we measured pressure (P)-volume (P-V) curves of regions with volumes of ∼1 cm3 in the dependent caudal lobes of oleic acid-injured dog lungs, during a very slow inflation from P = 0 to P = 30 cmH2O. The regional P-V curves are strongly sigmoidal. Regional volume, as a fraction of volume at total lung capacity, remains constant at 0.4–0.5 for airway P values from 0 to ∼20 cmH2O and then increases rapidly, but continuously, to 1 at P = ∼25 cmH2O. A model of parenchymal mechanics was modified to include the effects of elevated surface tension and fluid in t

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9

Wilson, Theodore A. "Parenchymal mechanics, gas mixing, and the slope of phase III." Journal of Applied Physiology 115, no. 1 (July 1, 2013): 64–70. http://dx.doi.org/10.1152/japplphysiol.00112.2013.

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A model of parenchymal mechanics is revisited with the objective of investigating the differences in parenchymal microstructure that underlie the differences in regional compliance that are inferred from gas-mixing studies. The stiffness of the elastic line elements that lie along the free edges of alveoli and form the boundary of the lumen of the alveolar duct is the dominant determinant of parenchymal compliance. Differences in alveolar size cause parallel shifts of the pressure-volume curve, but have little effect on compliance. However, alveolar size also affects the relation between surfa

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10

McCann, Ulysse G., Henry J. Schiller, Louis A. Gatto, Jay M. Steinberg, David E. Carney, and Gary F. Nieman. "Alveolar mechanics alter hypoxic pulmonary vasoconstriction*." Critical Care Medicine 30, no. 6 (June 2002): 1315–21. http://dx.doi.org/10.1097/00003246-200206000-00028.

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11

Hills, Brian A. "An alternative view of the role(s) of surfactant and the alveolar model." Journal of Applied Physiology 87, no. 5 (November 1, 1999): 1567–83. http://dx.doi.org/10.1152/jappl.1999.87.5.1567.

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Currently, the study of surfactant proteins is much in vogue, but, in the early days, the physics underlying surfactant function was treated somewhat superficially, leaving assumptions that have become culturally embedded, such as the “bubble” model of the alveolus. This review selectively reexamines these assumptions, comparing each combination of alveolar model and role of surfactant for compatibility with the major features of pulmonary mechanics and alveolar stability, morphology, and fluid balance.

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12

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.

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13

Wu, You, and Carrie E. Perlman. "In situ methods for assessing alveolar mechanics." Journal of Applied Physiology 112, no. 3 (February 1, 2012): 519–26. http://dx.doi.org/10.1152/japplphysiol.01098.2011.

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Lung mechanics are an important determinant of physiological and pathophysiological lung function. Recent light microscopy studies of the intact lung have furthered the understanding of lung mechanics but used methodologies that may have introduced artifacts. To address this concern, we employed a short working distance water immersion objective to capture confocal images of a fluorescently labeled alveolar field on the costal surface of the isolated, perfused rat lung. Surface tension held a saline drop between the objective tip and the lung surface, such that the lung surface was unconstrain

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14

Nieman, Gary, and Louis Gatto. "Dynamic alveolar mechanics in acute lung injury." Critical Care Medicine 38, no. 1 (January 2010): 344–45. http://dx.doi.org/10.1097/ccm.0b013e3181bfe74f.

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15

Mertens, Michael, Edmund Koch, and Wolfgang M. Kuebler. "Dynamic alveolar mechanics in acute lung injury." Critical Care Medicine 38, no. 1 (January 2010): 345. http://dx.doi.org/10.1097/ccm.0b013e3181c5464e.

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16

Bishai, John M., and Wayne Mitzner. "Effect of severe calorie restriction on the lung in two strains of mice." American Journal of Physiology-Lung Cellular and Molecular Physiology 295, no. 2 (August 2008): L356—L362. http://dx.doi.org/10.1152/ajplung.00514.2007.

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There is a body of literature in animal models that has suggested the development of emphysema following severe calorie restriction. This has led to the notion of “nutritional emphysema” that might have relevance in COPD patients. There have been few studies, however, that have looked closely at both the mechanics and lung structure in the same animals. In the present work, we examined lung mechanics and histological changes in two strains of mice that have substantial differences in alveolar size, the C57BL/6 and C3H/HeJ strains. We quantified the dynamic elastance and resistance at 2.5 Hz, t

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17

Massaro, Donald, and Gloria D. Massaro. "Invited Review: Pulmonary alveoli: formation, the “call for oxygen,” and other regulators." American Journal of Physiology-Lung Cellular and Molecular Physiology 282, no. 3 (March 1, 2002): L345—L358. http://dx.doi.org/10.1152/ajplung.00374.2001.

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The lung's only known essential function is to provide sufficient alveolar surface to meet the organism's need for oxygen and elimination of CO2. The importance of the magnitude of alveolar surface area (Sa) to O2uptake (V˙o2) is supported by the presence among mammals of a direct linear relationship between Sa and V˙o2. This match has been achieved, despite the higher body mass-specific V˙o2of small organisms compared with large, by a greater subdivision of alveolar surface, not by a larger relative lung volume in small organisms. This highly conserved relationship between alveolar architectu

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18

Nieman, Gary F., Josh Satalin, Michaela Kollisch-Singule, Penny Andrews, Hani Aiash, Nader M. Habashi, and Louis A. Gatto. "Physiology in Medicine: Understanding dynamic alveolar physiology to minimize ventilator-induced lung injury." Journal of Applied Physiology 122, no. 6 (June 1, 2017): 1516–22. http://dx.doi.org/10.1152/japplphysiol.00123.2017.

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Acute respiratory distress syndrome (ARDS) remains a serious clinical problem with the main treatment being supportive in the form of mechanical ventilation. However, mechanical ventilation can be a double-edged sword: if set improperly, it can exacerbate the tissue damage caused by ARDS; this is known as ventilator-induced lung injury (VILI). To minimize VILI, we must understand the pathophysiologic mechanisms of tissue damage at the alveolar level. In this Physiology in Medicine paper, the dynamic physiology of alveolar inflation and deflation during mechanical ventilation will be reviewed.

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19

Schiller, Henry J., Ulysse G. McCann, David E. Carney, Louis A. Gatto, Jay M. Steinberg, and Gary F. Nieman. "Altered alveolar mechanics in the acutely injured lung." Critical Care Medicine 29, no. 5 (May 2001): 1049–55. http://dx.doi.org/10.1097/00003246-200105000-00036.

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20

Lara, Irving Quezada, Rafael Alfredo Flores García, José R. Hernández Carvallo, and Karla Pérez Pérez. "Alveolar transportation through bone anchorage and sliding mechanics." Revista Mexicana de Ortodoncia 5, no. 3 (July 2017): e178-e183. http://dx.doi.org/10.1016/j.rmo.2017.12.017.

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21

Carney, David, Joseph DiRocco, and Gary Nieman. "Dynamic alveolar mechanics and ventilator-induced lung injury." Critical Care Medicine 33, Supplement (March 2005): S122—S128. http://dx.doi.org/10.1097/01.ccm.0000155928.95341.bc.

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22

Nieman, Gary F. "Amelia Earhart, alveolar mechanics, and other great mysteries." Journal of Applied Physiology 112, no. 6 (March 15, 2012): 935–36. http://dx.doi.org/10.1152/japplphysiol.01482.2011.

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23

Knudsen, Lars, Elena N. Atochina-Vasserman, Christopher B. Massa, Bastian Birkelbach, Chang-Jiang Guo, Pamela Scott, Beat Haenni, Michael F. Beers, Matthias Ochs, and Andrew J. Gow. "The role of inducible nitric oxide synthase for interstitial remodeling of alveolar septa in surfactant protein D-deficient mice." American Journal of Physiology-Lung Cellular and Molecular Physiology 309, no. 9 (November 1, 2015): L959—L969. http://dx.doi.org/10.1152/ajplung.00017.2015.

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Surfactant protein D (SP-D) modulates the lung's immune system. Its absence leads to NOS2-independent alveolar lipoproteinosis and NOS2-dependent chronic inflammation, which is critical for early emphysematous remodeling. With aging, SP-D knockout mice develop an additional interstitial fibrotic component. We hypothesize that this age-related interstitial septal wall remodeling is mediated by NOS2. Using invasive pulmonary function testing such as the forced oscillation technique and quasistatic pressure-volume perturbation and design-based stereology, we compared 29-wk-old SP-D knockout (Sftp

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24

Silage, D. A., and J. Gil. "Morphometric measurement of local curvature of the alveolar ducts in lung mechanics." Journal of Applied Physiology 65, no. 4 (October 1, 1988): 1592–97. http://dx.doi.org/10.1152/jappl.1988.65.4.1592.

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We have performed partial serial reconstructions of an acinus of the rabbit lung and determined the apparent existence of numerous heterogeneities in length, diameter, and local curvature in individual generation branches of the lung. We believe that structural changes during respiratory movements may include changes in the length and diameter of the whole duct. Alveoli are seen to be side differentiations secondary to the ducts in the gas-exchanging parenchyma of the rabbit lung. We have developed a technique for measuring local curvature in simple reconstructed ducts from the average of the

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25

Ryans, Jason M., Hideki Fujioka, and Donald P. Gaver. "Microscale to mesoscale analysis of parenchymal tethering: the effect of heterogeneous alveolar pressures on the pulmonary mechanics of compliant airways." Journal of Applied Physiology 126, no. 5 (May 1, 2019): 1204–13. http://dx.doi.org/10.1152/japplphysiol.00178.2018.

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In the healthy lung, bronchi are tethered open by the surrounding parenchyma; for a uniform distribution of these peribronchial structures, the solution is well known. An open question remains regarding the effect of a distributed set of collapsed alveoli, as can occur in disease. Here, we address this question by developing and analyzing microscale finite-element models of systems of heterogeneously inflated alveoli to determine the range and extent of parenchymal tethering effects on a neighboring collapsible airway. This analysis demonstrates that micromechanical stresses extend over a rang

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26

Tsuda, A., F. S. Henry, and J. P. Butler. "Chaotic mixing of alveolated duct flow in rhythmically expanding pulmonary acinus." Journal of Applied Physiology 79, no. 3 (September 1, 1995): 1055–63. http://dx.doi.org/10.1152/jappl.1995.79.3.1055.

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We examined the effects of rhythmic expansion of alveolar walls on fluid mechanics in the pulmonary acinus. We generated a realistic geometric model of an alveolated duct that expanded and contracted in a geometrically similar fashion to simulate tidal breathing. Time-dependent volumetric flow was generated by adjusting the proximal and distal boundary conditions. The low Reynolds number velocity field was solved numerically over the physiological range. We found that for a given geometry, the ratio of the alveolar flow (QA) to the ductal flow (QD) played a major role in determining the flow p

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27

Smith, T. C., and J. J. Marini. "Impact of PEEP on lung mechanics and work of breathing in severe airflow obstruction." Journal of Applied Physiology 65, no. 4 (October 1, 1988): 1488–99. http://dx.doi.org/10.1152/jappl.1988.65.4.1488.

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Positive end-expiratory pressure (PEEP) has generally been withheld from the treatment of patients with chronic airflow obstruction (CAO), in view of the risk of hyperinflation and lack of documented benefit. We studied 10 mechanically ventilated patients with exacerbated CAO and air trapping to determine the impact of PEEP on lung mechanics, alveolar pressure, and the work of breathing. PEEP levels of 5 and 10 cmH2O were applied to patients whose end-expiratory alveolar pressures were documented to be positive when breathing against ambient pressure (the auto-PEEP effect). All patients were s

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28

Subramaniam, K., H. Kumar, and M. H. Tawhai. "Evidence for age-dependent air-space enlargement contributing to loss of lung tissue elastic recoil pressure and increased shear modulus in older age." Journal of Applied Physiology 123, no. 1 (July 1, 2017): 79–87. http://dx.doi.org/10.1152/japplphysiol.00208.2016.

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As a normal part of mature aging, lung tissue undergoes microstructural changes such as alveolar air-space enlargement and redistribution of collagen and elastin away from the alveolar duct. The older lung also experiences an associated decrease in elastic recoil pressure and an increase in specific tissue elastic moduli, but how this relates mechanistically to microstructural remodeling is not well-understood. In this study, we use a structure-based mechanics analysis to elucidate the contributions of age-related air-space enlargement and redistribution of elastin and collagen to loss of lung

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29

Mathru, M. "Dynamic alveolar mechanics in four models of lung injury." Yearbook of Anesthesiology and Pain Management 2007 (January 2007): 135–36. http://dx.doi.org/10.1016/s1073-5437(08)70123-2.

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30

DiRocco, Joseph D., Lucio A. Pavone, David E. Carney, Charles J. Lutz, Louis A. Gatto, Steve K. Landas, and Gary F. Nieman. "Dynamic alveolar mechanics in four models of lung injury." Intensive Care Medicine 32, no. 1 (December 2, 2005): 140–48. http://dx.doi.org/10.1007/s00134-005-2854-3.

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31

Martin, Erica L., Tanya A. Sheikh, Kevin J. Leco, James F. Lewis, and Ruud A. W. Veldhuizen. "Contribution of alveolar macrophages to the response of the TIMP-3 null lung during a septic insult." American Journal of Physiology-Lung Cellular and Molecular Physiology 293, no. 3 (September 2007): L779—L789. http://dx.doi.org/10.1152/ajplung.00442.2006.

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Mice deficient in tissue inhibitor of metalloproteinase-3 (TIMP-3) develop an emphysema-like phenotype involving increased pulmonary compliance, tissue degradation, and matrix metalloproteinase (MMP) activity. After a septic insult, they develop a further increase in compliance that is thought to be a result of heightened metalloproteinase activity produced by the alveolar macrophage, potentially modeling an emphysemic exacerbation. Therefore, we hypothesized that TIMP-3 null mice lacking alveolar macrophages would not be susceptible to the altered lung function associated with a septic insult

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32

Steinberg, Jay, Henry J. Schiller, Jeffrey M. Halter, Louis A. Gatto, Monica Dasilva, Marcelo Amato, Ulysse G. McCann, and Gary F. Nieman. "Tidal volume increases do not affect alveolar mechanics in normal lung but cause alveolar overdistension and exacerbate alveolar instability after surfactant deactivation." Critical Care Medicine 30, no. 12 (December 2002): 2675–83. http://dx.doi.org/10.1097/00003246-200212000-00011.

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33

Staffieri, F., V. De Monte, C. De Marzo, F. Scrascia, and A. Crovace. "Alveolar recruiting maneuver in dogs under general anesthesia: effects on alveolar ventilation, gas exchange, and respiratory mechanics." Veterinary Research Communications 34, S1 (May 2, 2010): 131–34. http://dx.doi.org/10.1007/s11259-010-9405-2.

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34

Suki, B., H. Parameswaran, and A. Majumdar. "Lung tissue mechanics: from extracellular matrix to alveolar network behavior." Journal of Biomechanics 39 (January 2006): S267. http://dx.doi.org/10.1016/s0021-9290(06)84021-2.

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35

Féréol, Sophie, Redouane Fodil, Gabriel Pelle, Bruno Louis, and Daniel Isabey. "Cell mechanics of alveolar epithelial cells (AECs) and macrophages (AMs)." Respiratory Physiology & Neurobiology 163, no. 1-3 (November 2008): 3–16. http://dx.doi.org/10.1016/j.resp.2008.04.018.

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36

Dotta, A., S. Palamides, F. Crescenzi, A. Braguglia, and M. Orzalesi. "Broncho-Alveolar Lavage (BAL) and Lung Mechanics in Ventilated Newborns." Pediatric Research 45, no. 6 (June 1999): 889. http://dx.doi.org/10.1203/00006450-199906000-00033.

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37

Antonaglia, Vittorio, Massimo Ferluga, Nicola Bianco, Pier Paolo Accolla, and Walter A. Zin. "Respiratory mechanics during repeated lung lavages in pulmonary alveolar proteinosis." Internal and Emergency Medicine 7, S2 (March 17, 2012): 109–11. http://dx.doi.org/10.1007/s11739-012-0767-z.

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38

Sly, P. D., and C. J. Lanteri. "Site of action of hypertonic saline in the canine lung." Journal of Applied Physiology 71, no. 4 (October 1, 1991): 1315–21. http://dx.doi.org/10.1152/jappl.1991.71.4.1315.

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The site of action of inhaled hypertonic saline was determined in 8- to 10-wk-old puppies by combining measurements of respiratory mechanics, made during mechanical ventilation and after midexpiratory flow interruptions, with direct measurements of alveolar pressure. Under both control conditions and after inhalation of 10% saline, we were able to partition lung mechanics into components representing the airways and tissue viscoelastic properties. Hypertonic saline challenge altered lung mechanics by increasing airway resistance and did not have any effect on elastic or viscoelastic properties

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Arold, Stephen P., Béla Suki, Adriano M. Alencar, Kenneth R. Lutchen, and Edward P. Ingenito. "Variable ventilation induces endogenous surfactant release in normal guinea pigs." American Journal of Physiology-Lung Cellular and Molecular Physiology 285, no. 2 (August 2003): L370—L375. http://dx.doi.org/10.1152/ajplung.00036.2003.

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Variable or noisy ventilation, which includes random breath-to-breath variations in tidal volume (Vt) and frequency, has been shown to consistently improve blood oxygenation during mechanical ventilation in various models of acute lung injury. To further understand the effects of variable ventilation on lung physiology and biology, we mechanically ventilated 11 normal guinea pigs for 3 h using constant-Vt ventilation ( n = 6) or variable ventilation ( n = 5). After 3 h of ventilation, each animal underwent whole lung lavage for determination of alveolar surfactant content and composition, whil

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40

Pillow, J. Jane, Alan H. Jobe, Rachel A. Collins, Zoltán Hantos, Machiko Ikegami, Timothy J. M. Moss, John P. Newnham, Karen E. Willet, and Peter D. Sly. "Variability in preterm lamb lung mechanics after intra-amniotic endotoxin is associated with changes in surfactant pool size and morphometry." American Journal of Physiology-Lung Cellular and Molecular Physiology 287, no. 5 (November 2004): L992—L998. http://dx.doi.org/10.1152/ajplung.00158.2004.

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Antenatal exposure to intra-amniotic (IA) endotoxin initiates a complex series of events, including an inflammatory cascade, increased surfactant production, and alterations to lung structure. Using the low frequency forced oscillation technique as a sensitive tool for measurement of respiratory impedance, we aimed to determine which factors contributed most to measured changes in lung mechanics. Respiratory impedance data obtained from sedated preterm lambs exposed to either IA injection with saline or 20 mg of endotoxin 1, 2, 4, and 15 days before delivery at 125 days gestation were studied,

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41

Azeloglu, Evren U., Jahar Bhattacharya, and Kevin D. Costa. "Atomic force microscope elastography reveals phenotypic differences in alveolar cell stiffness." Journal of Applied Physiology 105, no. 2 (August 2008): 652–61. http://dx.doi.org/10.1152/japplphysiol.00958.2007.

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To understand the connection between alveolar mechanics and key biochemical events such as surfactant secretion, one first needs to characterize the underlying mechanical properties of the lung parenchyma and its cellular constituents. In this study, the mechanics of three major cell types from the neonatal rat lung were studied; primary alveolar type I (AT1) and type II (AT2) epithelial cells and lung fibroblasts were isolated using enzymatic digestion. Atomic force microscopy indentation was used to map the three-dimensional distribution of apparent depth-dependent pointwise elastic modulus.

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42

Bayindir, Osman, Belhhan Akpinar, Ug'ur Özbek, Emine Cakali, Ülkü Pekcan, Füsun Bulutçu, and Bingür Sönmez. "The hazardous effects of alveolar hypocapnia on lung mechanics during weaning from cardiopulmonary bypass." Perfusion 15, no. 1 (January 2000): 27–31. http://dx.doi.org/10.1177/026765910001500105.

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The bronchoconstrictive effects of alveolar hypocapnia during weaning from cardiopulmonary bypass (CPB) were investigated in patients undergoing elective coronary artery revascularization. Thirty patients were randomly assigned into two equal groups. In both groups, mechanical ventilation was initiated for 3 min prior to weaning from CPB with the venous pressure low. This kept the pulmonary vascular bed empty, resulting in alveolar hypocapnia (ETCO2 < 2 kPa). Peak airway pressure ( Ppeak) and plateau pressures ( Pplateau) were recorded. In group 1, 5% CO2 was added to the inspiratory gas mi

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Sly, P. D., and C. J. Lanteri. "Partitioning of pulmonary responses to inhaled methacholine in puppies." Journal of Applied Physiology 71, no. 3 (September 1, 1991): 886–91. http://dx.doi.org/10.1152/jappl.1991.71.3.886.

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Twelve open-chest mongrel puppies, 8–10 wk old, were studied to localize the site of action of inhaled methacholine within the lungs. Six puppies were challenged with methacholine aerosols and six were challenged with an equal number of nebulizations of normal saline (control group). Pulmonary mechanics were measured during mechanical ventilation and after midexpiratory flow interruptions. Alveolar pressure was measured to allow the partitioning of pulmonary mechanics into airway and tissue components. Good matching between airway opening and alveolar pressures was seen throughout the study. A

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Grieco, Domenico Luca, Gian Marco Anzellotti, Andrea Russo, Filippo Bongiovanni, Barbara Costantini, Marco D’Indinosante, Francesco Varone, et al. "Airway Closure during Surgical Pneumoperitoneum in Obese Patients." Anesthesiology 131, no. 1 (July 1, 2019): 58–73. http://dx.doi.org/10.1097/aln.0000000000002662.

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AbstractEditor’s PerspectiveWhat We Already Know about This TopicWhat This Article Tells Us That Is NewBackgroundAirway closure causes lack of communication between proximal airways and alveoli, making tidal inflation start only after a critical airway opening pressure is overcome. The authors conducted a matched cohort study to report the existence of this phenomenon among obese patients undergoing general anesthesia.MethodsWithin the procedures of a clinical trial during gynecological surgery, obese patients underwent respiratory/lung mechanics and lung volume assessment both before and afte

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Williams, Ian, and Todd M. Squires. "Evolution and mechanics of mixed phospholipid fibrinogen monolayers." Journal of The Royal Society Interface 15, no. 141 (April 2018): 20170895. http://dx.doi.org/10.1098/rsif.2017.0895.

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All mammals depend on lung surfactant (LS) to reduce surface tension at the alveolar interface and facilitate respiration. The inactivation of LS in acute respiratory distress syndrome (ARDS) is generally accompanied by elevated levels of fibrinogen and other blood plasma proteins in the alveolar space. Motivated by the mechanical role fibrinogen may play in LS inactivation, we measure the interfacial rheology of mixed monolayers of fibrinogen and dipalmitoylphosphatidylcholine (DPPC), the main constituent of LS, and compare these to the single species monolayers. We find DPPC to be ineffectiv

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Fitz-Clarke, John R. "Mechanics of airway and alveolar collapse in human breath-hold diving." Respiratory Physiology & Neurobiology 159, no. 2 (November 2007): 202–10. http://dx.doi.org/10.1016/j.resp.2007.07.006.

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Bickenbach, Johannes, Rolf Dembinski, Michael Czaplik, Sven Meissner, Arata Tabuchi, Michael Mertens, Lila Knels, et al. "Comparison of two in vivo microscopy techniques to visualize alveolar mechanics." Journal of Clinical Monitoring and Computing 23, no. 5 (September 3, 2009): 323–32. http://dx.doi.org/10.1007/s10877-009-9200-1.

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Pavone, Lucio A., Scott Albert, David Carney, Louis A. Gatto, Jeffrey M. Halter, and Gary F. Nieman. "Injurious mechanical ventilation in the normal lung causes a progressive pathologic change in dynamic alveolar mechanics." Critical Care 11, no. 3 (2007): R64. http://dx.doi.org/10.1186/cc5940.

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Nucci, Gianluca, Simonluca Tessarin, and Claudio Cobelli. "A Morphometric Model of Lung Mechanics for Time-Domain Analysis of Alveolar Pressures during Mechanical Ventilation." Annals of Biomedical Engineering 30, no. 4 (April 2002): 537–45. http://dx.doi.org/10.1114/1.1475344.

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Habre, Walid, Johannes H. Wildhaber, and Peter D. Sly. "Prevention of Methacholine-induced Changes in Respiratory Mechanics in Piglets." Anesthesiology 87, no. 3 (September 1, 1997): 585–90. http://dx.doi.org/10.1097/00000542-199709000-00019.

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Background Sevoflurane is a new volatile anesthetic agent that may be a useful alternative to halothane for anesthesia in children. However, there is insufficient information about its effects on respiratory mechanics, particularly in the presence of constrictor stimuli. Methods Eighteen piglets had anesthesia induced and maintained with either pentobarbital (control: n = 8), 1 minimum alveolar concentration (MAC) sevoflurane (sevo: n = 5), or 1 MAC halothane (halo: n = 5). Pressure, flow, and volume were measured at the airway opening and used to calculate lung compliance (C(L)) and resistanc

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