Journal articles: 'Alveolar mechanics'

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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, i.e., their walls are flat, and Laplace law considerations in their inflation apply only to the very small curved region in the fluid where these walls intersect. Alveoli do not readily collapse into one another because they are suspended in a matrix of connective tissue “cables” and share common, often perforated walls, so there can be no pressure differential across them. Surfactant has important functions along planar surfaces of the alveolar wall and in mitigating the forces that tend to close the small airways. Laplace’s law as it applies to cylinders is an important feature of the mechanics of airway collapse, but the law as it applies to spheres is not relevant to the individual alveolus.

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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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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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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 was a better correlation of sphericity rather than circularity with alveolar compliance. The compliance of clusters with great shape change was larger than that with relatively slight shape change. These findings suggest the contribution of lung heterogeneous expansion to lung injuries associated with mechanical ventilation.

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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 neighboring structures. Acinar volume was not a linear function of lung volume. The alveolar duct diameter changed dramatically during inflation at low pressures and remained relatively constant above an airway pressure of ∼8 cmH2O during inflation. The ratio of acinar surface area to acinar volume indicates that acinar distension during low-pressure inflation differed from that during inflation over a higher pressure range; in particular, acinar deformation was accordion-like during low-pressure inflation. These results indicated that the alveoli and duct expand differently as total acinar volume increases and that the alveolar duct may expand predominantly during low-pressure inflation. Our findings suggest that acinar deformation in the core regions of the lung is complex and heterogeneous.

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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, and inflammation. However, despite substantial advances in our understanding of lung mechanics over the last half century, there are still many unanswered questions regarding the micromechanics of the alveolus and how it deforms during lung inflation. Therefore, the aims of this review are to draw a multidisciplinary account of the mechanics of the alveolus on the basis of its structure, biology, and chemistry and to compare estimates of alveolar deformation from previous studies.

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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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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 the alveolar spaces. P-V curves calculated from the model are similar to the measured P-V curves. At lower lung volumes, P increases rapidly with lung volume as the air-fluid interface penetrates the mouth of the alveolus. At a value of P = ∼20 cmH2O, the air-fluid interface is inside the alveolus and the lung is compliant, like an air-filled lung with constant surface tension. We conclude that the properties of the P-V curve of edematous lungs, particularly the knee in the P-V curve, are the result of the mechanics of parenchyma with constant surface tension and partially fluid-filled alveoli, not the result of abrupt opening of airways or atelectatic parenchyma.

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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 surface tension and pressure during the breathing cycle. Thus regional differences in alveolar size generate regional differences in surface tension, and these drive Marangoni surface flows that equilibrate surface tension between neighboring acini. Surface tension relaxation introduces phase differences in regional volume oscillations and a dependence of expired gas concentration on expired volume. A particular example of different parenchymal properties in two neighboring acini is described, and gas exchange in this model is calculated. The efficiency of mixing and slope of phase III for the model agree well with published data. This model constitutes a new hypothesis concerning the origin of phase III.

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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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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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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 unconstrained. For comparison, we also imaged with O-ring and coverslip; with O-ring, coverslip, and vacuum pressure; and without perfusion. Under each condition, we ventilated the lung and imaged the same region at the endpoints of ventilation. We found use of a coverslip caused a minimal enlargement of the alveolar field; additional use of vacuum pressure caused no further dimensional change; and absence of perfusion did not affect alveolar field dimension. Inflation-induced expansion was unaltered by methodology. In response to inflation, percent expansion was the same as recorded by all four alternative methods.

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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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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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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, the quasistatic pressure volume curve, and the alveolar chord lengths in lungs inflated to a lung capacity at 25–30 cmH2O. We found that after 2 or 3 wk of calorie restriction to 1/3 their normal diet, the lungs became stiffer with increased resistance. In addition, the lung capacity was also decreased. These mechanical changes were reversed after 2 wk on a normal ad libitum diet. Histology of the postmortem fixed lungs showed no changes in the mean alveolar chord lengths with calorie restriction. Although the baseline mechanics and alveolar size were quantitatively different in the two strains, both strains showed similar qualitative changes during the starvation and refeeding periods. Thus, in two strains of mice with genetically determined differences in alveolar size, neither the mechanics nor the histology show any evidence of emphysema-like changes with this severe caloric insult.

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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 architecture and V˙o2suggests the presence of similarly conserved mechanisms that control the onset, rate, and cessation of alveolus formation and alveolar size, which are also influenced by retinoids and thyroid and corticosteroid hormones. Furthermore, the “call for oxygen” is met at a breathing rate and tidal volume at which the work of breathing is lowest. Thus there is a complex, fascinating, but poorly understood, signaling relationship among V˙o2, the neural regulation of breathing, and lung architecture, composition, and mechanics.

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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. In addition, the pathophysiologic mechanisms of VILI will be reviewed, and this knowledge will be used to suggest an optimal mechanical breath profile (MBP: all airway pressures, volumes, flows, rates, and the duration that they are applied at both inspiration and expiration) necessary to minimize VILI. Our review suggests that the current protective ventilation strategy, known as the “open lung strategy,” would be the optimal lung-protective approach. However, the viscoelastic behavior of dynamic alveolar inflation and deflation has not yet been incorporated into protective mechanical ventilation strategies. Using our knowledge of dynamic alveolar mechanics (i.e., the dynamic change in alveolar and alveolar duct size and shape during tidal ventilation) to modify the MBP so as to minimize VILI will reduce the morbidity and mortality associated with ARDS.

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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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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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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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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 (Sftpd−/−) mice, SP-D/NOS2 double-knockout (DiNOS) mice, and wild-type mice (WT). Structural changes, including alveolar epithelial surface area, distribution of septal wall thickness, and volumes of septal wall components (alveolar epithelium, interstitial tissue, and endothelium) were quantified. Twenty-nine-week-old Sftpd−/− mice had preserved lung mechanics at the organ level, whereas elastance was increased in DiNOS. Airspace enlargement and loss of surface area of alveolar epithelium coexist with increased septal wall thickness in Sftpd−/− mice. These changes were reduced in DiNOS, and compared with Sftpd−/− mice a decrease in volumes of interstitial tissue and alveolar epithelium was found. To understand the effects of lung pathology on measured lung mechanics, structural data were used to inform a computational model, simulating lung mechanics as a function of airspace derecruitment, septal wall destruction (loss of surface area), and septal wall thickening. In conclusion, NOS2 mediates remodeling of septal walls, resulting in deposition of interstitial tissue in Sftpd−/−. Forward modeling linking structure and lung mechanics describes the complex mechanical properties by parenchymatous destruction (emphysema), interstitial remodeling (septal wall thickening), and altered recruitability of acinar airspaces.

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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 integral curvation of the section contour. The contour curvature is measured from the chain code representation of the sampled contour from digital image analysis. The stereological requirements of an unbiased and random selection of contours is approached here by the random orientation of the individual alveoli of a single duct. Over 700 sections through the last four airway generations (alveolar ducts) at 3-micron intervals were analyzed. The average integral curvature ranges from 7.7 to 9.5 (mean 8.9) mm-1 for sixth- and seventh-generation branches from the start with volumes for the segments from 0.022 to 1.198 (mean 0.497) mm3.

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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 range of ∼5 airway radii, and this behavior is dictated primarily by the fraction, not distribution, of collapsed alveoli in that region. A mesoscale analysis of the microscale data identifies an effective shear modulus, Geff, that accurately characterizes the parenchymal support as a function of the average transpulmonary pressure of the surrounding alveoli. We demonstrate the use of this formulation by analyzing a simple model of a single collapsible airway surrounded by heterogeneously inflated alveoli (a “pig-in-a-blanket” model), which quantitatively demonstrates the increased parenchymal compliance and reduction in airway caliber that occurs with decreased parenchymal support from hypoinflated obstructed alveoli. This study provides a building block from which models of an entire lung can be developed in a computationally tenable manner that would simulate heterogeneous pulmonary mechanical interdependence. Such multiscale models could provide fundamental insight toward the development of protective ventilation strategies to reduce the incidence or severity of ventilator-induced lung injury. NEW & NOTEWORTHY A destabilized lung leads to airway and alveolar collapse that can result in catastrophic pulmonary failure. This study elucidates the micromechanical effects of alveolar collapse and determines its range of influence on neighboring collapsible airways. A mesoscale analysis reveals a master relationship that can that can be used in a computationally efficient manner to quantitatively model alveolar mechanical heterogeneity that exists in acute respiratory distress syndrome (ARDS), which predisposes the lung to volutrauma and/or atelectrauma. This analysis may lead to computationally tenable simulations of heterogeneous organ-level mechanical interactions that can illuminate novel protective ventilation strategies to reduce ventilator-induced lung injury.

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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 pattern. For larger QA/QD (as in the distal region in the acinus), the flow in the alveolus was largely radial. For small QA/QD (as in the proximal region in the acinus), the flow in the alveolus was slowly rotating and the velocity field near the alveolar opening was complex with a stagnation saddle point typical of chaotic flow structures. Performing Lagrangian fluid particle tracking, we demonstrated that in such a flow structure the motion of fluid could be highly complex, irreversible, and unpredictable even though it was governed by simple deterministic equations. These are the characteristics of chaotic flow behavior. We conclude that because of the unique geometry of alveolated duct and its time-dependent motion associated with tidal breathing, chaotic flow and chaotic mixing can occur in the lung periphery. Based on these novel observations, we suggest a new approach for studying acinar fluid mechanics and aerosol kinetics.

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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 studied under two conditions: every breath machine assisted (AMV) and every breath machine controlled (paralyzed, CMV). PEEP improved expiratory resistance without substantially increasing peak static pressure. Inspiratory resistance remained unchanged. The difference between the end-expiratory values of alveolar and central airway pressure narrowed as PEEP increased. Adding PEEP improved the effective triggering sensitivity of the ventilator, diminished ventilatory drive, and reduced the mechanical work of breathing during the machine-assisted ventilatory cycle. Our results indicate that low levels of PEEP may improve lung mechanics and reduce the effort required of mechanically ventilated patients with severe airflow obstruction, without substantially increasing the hazards of hyperinflation.

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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 elastic recoil pressure and increase in tissue elastic moduli. Our results show that age-related geometric changes can result in reduction of elastic recoil pressure and increase in shear and bulk moduli, which is consistent with published experimental data. All elastic moduli were sensitive to the distribution of stiffness (representing elastic fiber density) in the alveolar wall, with homogenous stiffness near the duct and through the septae resulting in a more compliant tissue. The preferential distribution of elastic proteins around the alveolar duct in the healthy young adult lung therefore provides for a more elastic tissue. NEW & NOTEWORTHY We use a structure-based mechanics analysis to correlate air-space enlargement and redistribution of elastin and collagen to age-related changes in the mechanical behavior of lung parenchyma. Our study highlights that both the cause (redistribution of elastin and collagen) and the structural effect (alveolar air-space enlargement) contribute to decline in lung tissue elastic recoil with age; these results are consistent with published data and provide a new avenue for understanding the mechanics of the older lung.

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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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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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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. TIMP-3 null and wild-type (WT) mice were depleted of alveolar macrophages before the induction of a septic insult and assessed for alteration in lung mechanics, alveolar structure, metalloproteinase levels, and inflammation. The results showed that TIMP-3 null mice lacking alveolar macrophages were protected from sepsis-induced alterations in lung mechanics, particularly pulmonary compliance, a finding that was supported by changes in alveolar structure. Additionally, changes in lung mechanics involved primarily peripheral tissue vs. central airways as determined using the flexiVent system. From investigation into possible molecules that could cause these alterations, it was found that although several proteases and inflammatory mediators were increased during the septic response, only MMP-7 was attenuated after macrophage depletion. In conclusion, the alveolar macrophage is essential for the TIMP-3 null sepsis-induced compliance alterations. This response may be mediated in part by MMP-7 activity but occurs independently of inflammatory cytokine and/or chemokine concentrations.

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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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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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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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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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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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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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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 of the lung.

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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, while protein content was assayed as a possible marker of injury. Another group of animals underwent whole lung lavage in the absence of mechanical ventilation to serve as an unventilated control group ( n = 5). Although lung mechanics did not vary significantly between groups, we found that variable ventilation improved oxygenation, increased surfactant levels nearly twofold, and attenuated alveolar protein content compared with animals ventilated with constant Vt. These data demonstrate that random variations in Vt promote endogenous release of biochemically intact surfactant, which improves alveolar stability, apparently reducing lung injury.

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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, and association with indexes of standard lung morphometry, inflammatory response, and alveolar surfactant-saturated phosphatidylcholine (Sat PC) pool size was demonstrated. Reduction in tissue impedance with increasing interval between exposure and delivery was evident as early as 4 days after IA endotoxin injection, coinciding with resolution of inflammatory reaction, increased alveolar surfactant pools, and contribution of alveolar ducts to the parenchymal fraction, and a later decrease in the tissue component of the parenchymal fraction. Decreases in tissue damping (resistance) were more marked than decreases in tissue elastance. Log alveolar Sat PC accounted for most variability in tissue damping (88.9%) and tissue elastance (73.4%), whereas tissue fraction contributed 2 and 6.4%, respectively. The alveolar Sat PC pool size was the sole factor contributing to change in tissue hysteresivity. No changes were observed in airway resistance. Despite the complex cascade of events initiated by antenatal endotoxin exposure, variability in lung tissue mechanics is associated primarily with changes in alveolar Sat PC pool and lung morphology.

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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. Histograms of apparent modulus data from all three cell types indicated non-Gaussian distributions that were highly skewed and appeared multimodal for AT2 cells and fibroblasts. Nuclear stiffness in all three cell types was similar (2.5 ± 1.0 kPa in AT1 vs. 3.1 ± 1.5 kPa in AT2 vs. 3.3 ± 0.8 kPa in fibroblasts; n = 10 each), whereas cytoplasmic moduli were significantly higher in fibroblasts and AT2 cells (6.0 ± 2.3 and 4.7 ± 2.9 kPa vs. 2.5 ± 1.2 kPa). In both epithelial cell types, actin was arranged in sparse clusters, whereas prominent actin stress fibers were observed in lung fibroblasts. No systematic difference in actin or microtubule organization was noted between AT1 and AT2 cells. Atomic force microscope elastography, combined with live-cell fluorescence imaging, revealed that the stiffer measurements in AT2 cells often colocalized with lamellar bodies. These findings partially explain reported heterogeneity of alveolar cell deformation during in situ lung inflation and provide needed data for better understanding of how mechanical stretch influences surfactant release.

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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 mixture and the ETCO2 allowed to rise (ETCO2 > 3.3 kPa). The ventilation pressure measurements were recorded again after 3 min stabilization. In group 2, the venous pressure was increased to allow the pulmonary venous bed to fill and the ventilation pressures recorded after a 3 min period of stabilization. In group 1, the ventilatory pressures dropped significantly ( p < 0.001) when the alveolar hypocapnia was reversed with added CO2 ( Ppeak 19.71 ± 5.7 to 12.31 ± 2.8 cmH2O and Pplateau 13.15 ± 3.28 to 9.15 ± 2.23 cmH2O). In group 2, a similar effect was achieved by allowing filling of the pulmonary vascular bed ( Ppeak 17.46 ± 4.72 to 11.92 ± 3.03 cmH2O and Pplateau 13.93 ± 4.10 to 9.37 ± 3.00 cmH2O). These results suggest that filling the pulmonary vascular bed prior to initiating ventilation, when weaning from CPB, prevents the otherwise deleterious effects of alveolar hypocapnia, resulting in raised bronchomotor tonus and raised airway pressures.

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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. After methacholine challenge, lung resistance increased fivefold. Increases in airway resistance and in the parameters reflecting tissue viscoelastic properties contributed to this increase in lung resistance. Dynamic lung elastance also increased threefold. The response of the methacholine group was statistically different from that of the control group. These data indicate that both the airways and pulmonary parenchyma contribute to the response to inhaled methacholine in 8- to 10-wk-old puppies.

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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 after pneumoperitoneum, in the supine and Trendelenburg positions, respectively. Among patients included in this study, those exhibiting airway closure were compared to a control group of subjects enrolled in the same trial and matched in 1:1 ratio according to body mass index.ResultsEleven of 50 patients (22%) showed airway closure after intubation, with a median (interquartile range) airway opening pressure of 9 cm H2O (6 to 12). With pneumoperitoneum, airway opening pressure increased up to 21 cm H2O (19 to 28) and end-expiratory lung volume remained unchanged (1,294 ml [1,154 to 1,363] vs. 1,160 ml [1,118 to 1,256], P = 0.155), because end-expiratory alveolar pressure increased consistently with airway opening pressure and counterbalanced pneumoperitoneum-induced increases in end-expiratory esophageal pressure (16 cm H2O [15 to 19] vs. 27 cm H2O [23 to 30], P = 0.005). Conversely, matched control subjects experienced a statistically significant greater reduction in end-expiratory lung volume due to pneumoperitoneum (1,113 ml [1,040 to 1,577] vs. 1,000 ml [821 to 1,061], P = 0.006). With airway closure, static/dynamic mechanics failed to measure actual lung/respiratory mechanics. When patients with airway closure underwent pressure-controlled ventilation, no tidal volume was inflated until inspiratory pressure overcame airway opening pressure.ConclusionsIn obese patients, complete airway closure is frequent during anesthesia and is worsened by Trendelenburg pneumoperitoneum, which increases airway opening pressure and alveolar pressure: besides preventing alveolar derecruitment, this yields misinterpretation of respiratory mechanics and generates a pressure threshold to inflate the lung that can reach high values, spreading concerns on the safety of pressure-controlled modes in this setting.

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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 ineffective at displacing preadsorbed fibrinogen, which gives the resulting mixed monolayer a strongly elastic shear response. By contrast, how effectively a pre-existing DPPC monolayer prevents fibrinogen adsorption depends upon its surface pressure. At low DPPC surface pressures, fibrinogen penetrates DPPC monolayers, imparting a mixed viscoelastic shear response. At higher initial DPPC surface pressures, this response becomes increasingly viscous-dominated, and the monolayer retains a more fluid, DPPC-like character. Fluorescence microscopy reveals that the mixed monolayers exhibit qualitatively different morphologies. Fibrinogen has a strong, albeit preparation-dependent, mechanical effect on phospholipid monolayers, which may contribute to LS inactivation and disorders such as ARDS.

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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 resistance (R(L)). Resistance was partitioned into airway (Raw) and parenchymal (Vti) components using alveolar pressure. Methacholine was infused intravenously in a dose sufficient (15 microg x kg(-1) x h(-1)) to approximately double R(L). Results The increase in R(L) seen in the control group was almost entirely due to an increase in Vti. Sevoflurane and halothane prevented the increase in R(L) and Vti (both P < 0.02) and the decrease in C(L) (both P < 0.02). Conclusions Sevoflurane and halothane can prevent methacholine-induced changes in lung function.

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Journal articles on the topic 'Alveolar mechanics'

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