Relevant bibliographies by topics / Alveolar mechanics

Academic literature on the topic 'Alveolar mechanics'

Author: Grafiati
Published: 4 June 2021
Last updated: 19 February 2022

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Journal articles on the topic "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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Dissertations / Theses on the topic "Alveolar mechanics"

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Liu, Hui. "The application of alveolar microscope on alveolar mechanics of ventilator-induced lung injury." [S.l. : s.n.], 2008. http://nbn-resolving.de/urn:nbn:de:bsz:25-opus-61847.

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Dash, Shari Anne Ahmed El. "Estudo tomográfico de pressões de colapso alveolar e níveis isogravitacionais em pulmões de pacientes com SDRA e LPA." Universidade de São Paulo, 2009. http://www.teses.usp.br/teses/disponiveis/5/5159/tde-25062009-113611/.

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Estudo clínico prospectivo, em 11 pacientes com SARA ou LPA, avaliando o comportamento regional da densidade do tecido pulmonar e do colapso alveolar ao longo dos três eixos do espaço. Foram realizadas tomografias seriadas, após manobra de recrutamento inicial e após níveis de PEEP progressivamente decrescentes. Regressão linear múltipla (R2=0.83) mostrou importante gradiente no eixo gravitacional (p<0.001) e não no sentido céfalo-caudal (p<0.001), nem da direita para a esquerda (p<0.05). Isto corrobora o conceito do pulmão líquido, em que a resultante das pressões exercidas pelo diafragma, estruturas mediastinais e derrames seria transmitida uniformemente pelo tecido pulmonar. Cada um destes níveis isogravitacionais tem uma pressão crítica de fechamento (Pclosing), que é maior do que a pressão superimposta calculada. PEEP tem um efeito homogeneizador sobre o parênquima pulmonar. Dentre os parâmetros clínicos estudados, Pflex mostrou a pior correlação com colapso pulmonar documentado enquanto PO2 e a complacência máxima se mostraram equivalentes.
A prospective clinical study performed on 11 patients with ARDS or ALI with the intention of studying the regional behavior of lung tissue density and alveolar collapse along the three spatial axes. An initial recruitment maneuver was followed by multiple semi-complete CT scans at descending levels of PEEP. Multiple linear regression (R2=0.83) showed a gravitational gradient of densities and collapse (p<0.001) and no cephalo-caudal (p<0.001) or right-toleft increase (p<0.05), corroborating the liquid-like behavior of the lung. Pressure exerted by mediastinal structures, chest wall and effusions is transmitted uniformly throughout the lung. PEEP has a homogenizing effect on lung parenchyma. Among commonly used clinical surrogates, Pflex showed the worst correlation with actual lung collapse, while arterial PO2 and compliance were equivalent.
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Namati, Eman, and eman@namati com. "Pre-Clinical Multi-Modal Imaging for Assessment of Pulmonary Structure, Function and Pathology." Flinders University. Computer Science, Engineering and Mathematics, 2008. http://catalogue.flinders.edu.au./local/adt/public/adt-SFU20081013.044657.

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In this thesis, we describe several imaging techniques specifically designed and developed for the assessment of pulmonary structure, function and pathology. We then describe the application of this technology within appropriate biological systems, including the identification, tracking and assessment of lung tumors in a mouse model of lung cancer. The design and development of a Large Image Microscope Array (LIMA), an integrated whole organ serial sectioning and imaging system, is described with emphasis on whole lung tissue. This system provides a means for acquiring 3D pathology of fixed whole lung specimens with no infiltrative embedment medium using a purpose-built vibratome and imaging system. This system enables spatial correspondence between histology and non-invasive imaging modalities such as Computed Tomography (CT), Magnetic Resonance Imaging (MRI) and Positron Emission Tomography (PET), providing precise correlation of the underlying 'ground truth' pathology back to the in vivo imaging data. The LIMA system is evaluated using fixed lung specimens from sheep and mice, resulting in large, high-quality pathology datasets that are accurately registered to their respective CT and H&E histology. The implementation of an in vivo micro-CT imaging system in the context of pulmonary imaging is described. Several techniques are initially developed to reduce artifacts commonly associated with commercial micro-CT systems, including geometric gantry calibration, ring artifact reduction and beam hardening correction. A computer controlled Intermittent Iso-pressure Breath Hold (IIBH) ventilation system is then developed for reduction of respiratory motion artifacts in live, breathing mice. A study validating the repeatability of extracting valuable pulmonary metrics using this technique against standard respiratory gating techniques is then presented. The development of an ex vivo laser scanning confocal microscopy (LSCM) and an in vivo catheter based confocal microscopy (CBCM) pulmonary imaging technique is described. Direct high-resolution imaging of sub-pleural alveoli is presented and an alveolar mechanic study is undertaken. Through direct quantitative assessment of alveoli during inflation and deflation, recruitment and de-recruitment of alveoli is quantitatively measured. Based on the empirical data obtained in this study, a new theory on alveolar mechanics is proposed. Finally, a longitudinal mouse lung cancer study utilizing the imaging techniques described and developed throughout this thesis is presented. Lung tumors are identified, tracked and analyzed over a 6-month period using a combination of micro-CT, micro-PET, micro-MRI, LSCM, CBCM, LIMA and H&E histology imaging. The growth rate of individual tumors is measured using the micro-CT data and traced back to the histology using the LIMA system. A significant difference in tumor growth rates within mice is observed, including slow growing, regressive, disappearing and aggressive tumors, while no difference between the phenotype of tumors was found from the H&E histology. Micro-PET and micro-MRI imaging was conducted at the 6-month time point and revealed the limitation of these systems for detection of small lesions ( < 2mm) in this mouse model of lung cancer. The CBCM imaging provided the first high-resolution live pathology of this mouse model of lung cancer and revealed distinct differences between normal, suspicious and tumor regions. In addition, a difference was found between control A/J mice parenchyma and Urethane A/J mice ‘normal’ parenchyma, suggesting a 'field effect' as a result of the Urethane administration and/or tumor burden. In conclusion, a comprehensive murine lung cancer imaging study was undertaken, and new information regarding the progression of tumors over time has been revealed.
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Rolle, Trenicka. "Lung Alveolar and Tissue Analysis Under Mechanical Ventilation." VCU Scholars Compass, 2014. http://scholarscompass.vcu.edu/etd/3398.

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Mechanical ventilation has been a major therapy used by physicians in support of surgery as well as for treating patients with reduced lung function. Despite its many positive outcomes and ability to maintain life, in many cases, it has also led to increased injury of the lungs, further exacerbating the diseased state. Numerous studies have investigated the effects of long term ventilation with respect to lungs, however, the connection between the global deformation of the whole organ and the strains reaching the alveolar walls remains unclear. The walls of lung alveoli also called the alveolar septum are characterized as a multilayer heterogeneous biological tissue. In cases where damage to this parenchymal structure insist, alveolar overdistension occurs. Therefore, damage is most profound at the alveolar level and the deformation as a result of such mechanical forces must be investigated thoroughly. This study investigates a three-dimensional lung alveolar model from generations 22 (alveolar ducts) through 24 (alveoli sacs) in order to estimate the strain/stress levels under mechanical ventilation conditions. Additionally, a multilayer alveolar tissue model was generated to investigate localized damage at the alveolar wall. Using ANSYS, a commercial finite element software package, a fluid-structure interaction analysis (FSI) was performed on both models. Various cases were simulated that included a normal healthy lung, normal lung with structural changes to model disease and normal lung with mechanical property changes to model aging. In the alveolar tissue analysis, strains obtained from the aged lung alveolar analysis were applied as a boundary condition and used to obtain the mechanical forces exerted as a result. This work seeks to give both a qualitative and quantitative description of the stress/strain fields exerted at the alveolar region of the lungs. Regions of stress/strain concentration will be identified in order to gain perspective on where excess damage may occur. Such damage can lead to overdistension and possible collapse of a single alveolus. Furthermore, such regions of intensified stress/strain are translated to the cellular level and offset a signaling cascade. Hence, this work will provide distributions of mechanical forces across alveolar and tissue models as well as significant quantifications of damaging stresses and strains.
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Liao, Pinhu. "Mechanotransduction in alveolar epithelial cells subjected to mechanical strain." Thesis, Imperial College London, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.479153.

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Chen, Shanze [Verfasser], and Silke [Akademischer Betreuer] Meiners. "Molecular mechanism of alveolar macrophage polarization and cell communication with alveolar epithelial cell / Shanze Chen. Betreuer: Silke Meiners." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2015. http://d-nb.info/1080479074/34.

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McKechnie, Stuart R. "The roles of hyperoxia and mechanical deformation in alveolar epithelial injury and repair." Thesis, University of Edinburgh, 2008. http://hdl.handle.net/1842/2691.

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The alveolar epithelium is a key functional component of the air-blood barrier in the lung. Comprised of two morphologically distinct cell types, alveolar epithelial type I (ATI) and type II (ATII) cells, effective repair of the alveolar epithelial barrier following injury appears to be an important determinant of clinical outcome. The prevailing view suggests this repair is achieved by the proliferation of ATII cells and the transdifferentiation of ATII cells into ATI cells. Supplemental oxygen and mechanical ventilation are key therapeutic interventions in the supportive treatment of respiratory failure following lung injury, but the effects of hyperoxia and mechanical deformation in the injured lung, and on alveolar epithelial repair in particular, are largely unknown. The clinical impression however, is that poor outcome is associated with exposure of injured (repairing) epithelium to such iatrogenic ‘hits’. This thesis describes studies investigating the hypothesis that hyperoxia & mechanical deformation inhibit normal epithelial repair. The in vitro data presented demonstrate that hyperoxia reversibly inhibits the transdifferentiation of ATII-like cells into ATI-like cells with time in culture. Whilst confirming that hyperoxia is injurious to alveolar epithelial cells, these data further suggest the ATII cell population harbours a subpopulation of cells resistant to hyperoxia-induced injury. This subpopulation of cells appears to generate fewer reactive oxygen species and express lower levels of the zonula adherens protein E-cadherin. Using a panel of antibodies to ATI (RTI40) and ATII (MMC4 & RTII70) cell-selective proteins, the effect of hyperoxia on the phenotype of the alveolar epithelium in a rat model of resolving S. aureus-induced lung injury was investigated. These in vivo studies support the view that, under normoxic conditions, alveolar epithelial repair occurs through ATII cell proliferation & transdifferentiation of ATII cells into ATI cells, with transdifferentiation occurring via a novel intermediate (MMC4/RTI40-coexpressing) immunophenotype. However, in S. aureus-injured lungs exposed to hyperoxia, the resolution of ATII cell hyperplasia was impaired, with an increase in ATII cell-staining membrane and a reduction in intermediate cell-staining membrane compared to injured lungs exposed to normoxia alone. As hyperoxia is pro-apoptotic and known to inhibit ATII cell proliferation, these data support the hypothesis that hyperoxia impairs normal epithelial repair by inhibiting the transdifferentiation of ATII cells into ATI cells in vivo. The effect of mechanical deformation on alveolar epithelial cells in culture was investigated by examining changes in cell viability following exposure of epithelial cell monolayers to quantified levels of cyclic equibiaxial mechanical strain. In the central region of monolayers, deformation-induced injury was a non-linear function of deformation magnitude, with significant injury occurring only following exposure to strains greater than those associated with inflation of the intact lung to total lung capacity. However, these studies demonstrate for the first time that different epithelial cell phenotypes within the same culture system have different sensitivities to deformation-induced injury, with spreading RTI40-expressing cells in the peripheral region of epithelial cell monolayers and in the region of ‘repairing’ wounds being injured even at physiological levels of mechanical strain. These findings are consistent with the hypothesis that alveolar epithelial cells in regions of epithelial repair are highly susceptible to deformation-induced injury.
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Fois, Georgio [Verfasser]. "Response of alveolar type II pneumocytes to mechanical stimulation / Giorgio Fois." Ulm : Universität Ulm. Medizinische Fakultät, 2012. http://d-nb.info/1019167831/34.

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Dickie, A. John. "Mechanisms by which endotoxin-stimulated alveolar macrophages impair lung epithelial sodium transport." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape11/PQDD_0025/MQ51593.pdf.

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Mossadeq, Sayeed. "Kinetics and mechanisms of accumulation for liposomal ciprofloxacin into rat alveolar macrophages." VCU Scholars Compass, 2013. http://scholarscompass.vcu.edu/etd/501.

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The kinetics and mechanism of accumulation for liposomal ciprofloxacin (Lipo-CPFX) into the rat alveolar macrophage NR8383 cells were studied in vitro, in comparison to unformulated ciprofloxacin (CPFX). Upon incubation with CPFX or Lipo-CPFX, cellular drug accumulation was determined from the cell lysates or efflux was from the extracellular media by fluorescence-HPLC. The accumulation for Lipo-CPFX reached the asymptotic values at ≥ 2 hours, which was a result of uptake and efflux. The uptake appeared to be due to liposomes, mediated via cellular energy-independent mechanism like lipid fusion. In contrast, the efflux appeared to be due to ciprofloxacin, partly cellular energy-dependent, and involve probenecid-sensitive multidrug resistance proteins (MRPs). Overall, Lipo-CPFX enabled greater drug accumulation into the NR8383 cells than CPFX. This logically suggests a greater potential to treat respiratory infections especially caused by bacteria resistant to phagocytic killing.
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Books on the topic "Alveolar mechanics"

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Kreit, John W. Respiratory Mechanics. Edited by John W. Kreit. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190670085.003.0001.

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Ventilation can occur only when the respiratory system expands above and then returns to its resting or equilibrium volume. This is just another way of saying that ventilation depends on our ability to breathe. Although breathing requires very little effort and even less thought, it’s nevertheless a fairly complex process. Respiratory Mechanics reviews the interaction between applied and opposing forces during spontaneous and mechanical ventilation. It discusses elastic recoil, viscous forces, compliance, resistance, and the equation of motion and the time constant of the respiratory system. It also describes how and why pleural, alveolar, lung transmural, intra-abdominal, and airway pressure change during spontaneous and mechanical ventilation, and the effect of applied positive end-expiratory pressure (PEEP).
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Muders, Thomas, and Christian Putensen. Pressure-controlled mechanical ventilation. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0096.

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Beside reduction in tidal volume limiting peak airway pressure minimizes the risk for ventilator-associated-lung-injury in patients with acute respiratory distress syndrome. Pressure-controlled, time-cycled ventilation (PCV) enables the physician to keep airway pressures under strict limits by presetting inspiratory and expiratory pressures, and cycle times. PCV results in a square-waved airway pressure and a decelerating inspiratory gas flow holding the alveoli inflated for the preset time. Preset pressures and cycle times, and respiratory system mechanics affect alveolar and intrinsic positive end-expiratory (PEEPi) pressures, tidal volume, total minute, and alveolar ventilation. When compared with flow-controlled, time-cycled (‘volume-controlled’) ventilation, PCV results in reduced peak airway pressures, but higher mean airway. Homogeneity of regional peak alveolar pressure distribution within the lung is improved. However, no consistent data exist, showing PCV to improve patient outcome. During inverse ratio ventilation (IRV) elongation of inspiratory time increases mean airway pressure and enables full lung inflation, whereas shortening expiratory time causes incomplete lung emptying and increased PEEPi. Both mechanisms increase mean alveolar and transpulmonary pressures, and may thereby improve lung recruitment and gas exchange. However, when compared with conventional mechanical ventilation using an increased external PEEP to reach the same magnitude of total PEEP as that produced intrinsically by IRV, IRV has no advantage. Airway pressure release ventilation (APRV) provides a PCV-like squared pressure pattern by time-cycled switches between two continuous positive airway pressure levels, while allowing unrestricted spontaneous breathing in any ventilatory phase. Maintaining spontaneous breathing with APRV is associated with recruitment and improved ventilation of dependent lung areas, improved ventilation-perfusion matching, cardiac output, oxygenation, and oxygen delivery, whereas need for sedation, vasopressors, and inotropic agents and duration of ventilator support decreases.
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Martin-Loeches, Ignacio, and Antonio Artigas. Respiratory support with positive end-expiratory pressure. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0094.

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Positive-end-expiratory pressure (PEEP) is the pressure present in the airway (alveolar pressure) above atmospheric pressure that exists at the end of expiration. The term PEEP is defined in two particular settings. Extrinsic PEEP (applied by ventilator) and intrinsic PEEP (PEEP caused by non-complete exhalation causing progressive air trapping). Applied (extrinsic) PEEP—is usually one of the first ventilator settings chosen when mechanical ventilation (MV) is initiated. Applying PEEP increases alveolar pressure and volume. The increased lung volume increases the surface area by reopening and stabilizing collapsed or unstable alveoli. PEEP therapy can be effective when used in patients with a diffuse lung disease with a decrease in functional residual capacity. Lung protection ventilation is an established strategy of management to reduce and avoid ventilator-induced lung injury and mortality. Levels of PEEP have been traditionally used from 5 to 12 cmH2O; however, higher levels of PEEP have also been proposed and updated in order to keep alveoli open, without the cyclical opening and closing of lung units (atelectrauma). The ideal level of PEEP is that which prevents derecruitment of the majority of alveoli, while causing minimal overdistension; however, it should be individualized and higher PEEP might be used in the more severe end of the spectrum of patients with improved survival. A survival benefit for higher levels of PEEP has not been yet reported for any patient under MV, but a higher PaO2/FiO2 ratio seems to be better in the higher PEEP group.
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MacIntyre, Neil R. Indications for mechanical ventilation. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0091.

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Mechanical ventilation is indicated when the patient’s ability to ventilate the lung and/or effect gas transport across the alveolar capillary interface is compromised to point that harm is imminent. In practice, this means addressing one or more of three fundamental pathophysiological processes—loss of proper ventilatory control, ventilatory muscle demand-capability imbalances, and/or loss of alveolar patency. A fourth general indication involves providing a positive pressure assistance to allow tolerance of an artificial airway in the patient unable to maintain a patent and protected airway. The decision to initiate mechanical ventilation usually involves an integrated assessment that should include mental status, airway protection capabilities, ventilatory muscle load tolerance, spontaneous ventilatory pattern, and signs of organ dysfunction from either acidosis and/or hypoxaemia. Providing mechanical ventilatory assistance can be life-sustaining, but it is associated with significant risk, including ventilator-induced lung injury, infection, and need for sedatives/paralytics, and must be applied only when indications justify the risk.
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Ware, Lorraine B. Pathophysiology of acute respiratory distress syndrome. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0108.

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The acute respiratory distress syndrome (ARDS) is a syndrome of acute respiratory failure characterized by the acute onset of non-cardiogenic pulmonary oedema due to increased lung endothelial and alveolar epithelial permeability. Common predisposing clinical conditions include sepsis, pneumonia, severe traumatic injury, and aspiration of gastric contents. Environmental factors, such as alcohol abuse and cigarette smoke exposure may increase the risk of developing ARDS in those at risk. Pathologically, ARDS is characterized by diffuse alveolar damage with neutrophilic alveolitis, haemorrhage, hyaline membrane formation, and pulmonary oedema. A variety of cellular and molecular mechanisms contribute to the pathophysiology of ARDS, including exuberant inflammation, neutrophil recruitment and activation, oxidant injury, endothelial activation and injury, lung epithelial injury and/or necrosis, and activation of coagulation in the airspace. Mechanical ventilation can exacerbate lung inflammation and injury, particularly if delivered with high tidal volumes and/or pressures. Resolution of ARDS is complex and requires coordinated activation of multiple resolution pathways that include alveolar epithelial repair, clearance of pulmonary oedema through active ion transport, apoptosis, and clearance of intra-alveolar neutrophils, resolution of inflammation and fibrinolysis of fibrin-rich hyaline membranes. In some patients, activation of profibrotic pathways leads to significant lung fibrosis with resultant prolonged respiratory failure and failure of resolution.
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Lucangelo, Umberto, and Massimo Ferluga. Pulmonary mechanical dysfunction in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0084.

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In intensive care units practitioners are confronted every day with mechanically-ventilated patients and should be able to sort out from all the data available from modern ventilators to tailored patient ventilatory strategy. Real-time visualization of pressure, flow and tidal volume provide valuable information on the respiratory system, to optimize ventilatory support and avoiding complications associated with mechanical ventilation. Early determination of patient–ventilator asynchrony, air-trapping, and variation in respiratory parameters is important during mechanical ventilation. A correct evaluation of data becomes mandatory to avoid a prolonged need for ventilatory support. During dynamic hyperinflation the lungs do not have time to reach the functional residual capacity at the end of expiration, increasing the work of breathing and promoting patient-ventilator asynchrony. Expiratory capnogram provides qualitative information on the waveform patterns associated with mechanical ventilation and quantitative estimation of expired CO2. The concept of dead space accounts for those lung areas that are ventilated but not perfused. Calculations derived from volumetric capnography are useful indicators of pulmonary embolism. Moreover, alveolar dead space is increased in acute lung injury and its value decreased in case of positive end-expiratory pressure (PEEP)-induced recruitment, whereas PEEP-induced overdistension tends to increment alveolar dead space.
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Joynt, Gavin M., and Gordon Y. S. Choi. Blood gas analysis in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0072.

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Arterial blood gases allow the assessment of patient oxygenation, ventilation, and acid-base status. Blood gas machines directly measure pH, and the partial pressures of carbon dioxide (PaCO2) and oxygen (PaO2) dissolved in arterial blood. Oxygenation is assessed by measuring PaO2 and arterial blood oxygen saturation (SaO2) in the context of the inspired oxygen and haemoglobin concentration, and the oxyhaemoglobin dissociation curve. Causes of arterial hypoxaemia may often be elucidated by determining the alveolar–arterial oxygen gradient. Ventilation is assessed by measuring the PaCO2 in the context of systemic acid-base balance. A rise in PaCO2 indicates alveolar hypoventilation, while a decrease indicates alveolar hyperventilation. Given the requirement to maintain a normal pH, functioning homeostatic mechanisms result in metabolic acidosis, triggering a compensatory hyperventilation, while metabolic alkalosis triggers a compensatory reduction in ventilation. Similarly, when primary alveolar hypoventilation generates a respiratory acidosis, it results in a compensatory increase in serum bicarbonate that is achieved in part by kidney bicarbonate retention. In the same way, respiratory alkalosis induces kidney bicarbonate loss. Acid-base assessment requires the integration of clinical findings and a systematic interpretation of arterial blood gas parameters. In clinical use, traditional acid-base interpretation rules based on the bicarbonate buffer system or standard base excess estimations and the interpretation of the anion gap, are substantially equivalent to the physicochemical method of Stewart, and are generally easier to use at the bedside. The Stewart method may have advantages in accurately explaining certain physiological and pathological acid base problems.
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Hedenstierna, Göran, and Hans Ulrich Rothen. Physiology of positive-pressure ventilation. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0088.

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During positive pressure ventilation the lung volume is reduced because of loss of respiratory muscle tone. This promotes airway closure that occurs in dependent lung regions. Gas absorption behind the closed airway results sooner or later in atelectasis depending on the inspired oxygen concentration. The elevated airway and alveolar pressures squeeze blood flow down the lung so that a ventilation/perfusion mismatch ensues with more ventilation going to the upper lung regions and more perfusion going to the lower, dependent lung. Positive pressure ventilation may impede the return of venous blood to the thorax and right heart. This raises venous pressure, causing an increase in systemic capillary pressure with increased capillary leakage and possible oedema formation in peripheral organs. Steps that can be taken to counter the negative effects of mechanical ventilation include an increase in lung volume by recruitment of collapsed lung and an appropriate positive end-expiratory pressure, to keep aerated lung open and to prevent cyclic airway closure. Maintaining normo- or hypervolaemia to make the pulmonary circulation less vulnerable to increased airway and alveolar pressures, and preserving or mimicking spontaneous breaths, in addition to the mechanical breaths, since they may improve matching of ventilation and blood flow, may increase venous return and decrease systemic organ oedema formation (however, risk of respiratory muscle fatigue, and even overexpansion of lung if uncontrolled).
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Cuartero, Mireia, and Niall D. Ferguson. High-frequency ventilation and oscillation. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0098.

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High-frequency oscillatory ventilation (HFOV) is a key member of the family of modes called high-frequency ventilation and achieves adequate alveolar ventilation despite using very low tidal volumes, often below the dead space volume, at frequencies significantly above normal physiological values. It has been proposed as a potential protective ventilatory strategy, delivering minimal alveolar tidal stretch, while also providing continuous lung recruitment. HFOV has been successfully used in neonatal and paediatric intensive care units over the last 25 years. Since the late 1990s adults with acute respiratory distress syndrome have been treated using HFOV. In adults, several observational studies have shown improved oxygenation in patients with refractory hypoxaemia when HFOV was used as rescue therapy. Several small older trials had also suggested a mortality benefit with HFOV, but two recent randomized control trials in adults with ARDS have shed new light on this area. These trials not show benefit, and in one of them a suggestion of harm was seen with increased mortality for HFOV compared with protective conventional mechanical ventilation strategies (tidal volume target 6 mL/kg with higher positive end-expiratory pressure). While these findings do not necessarily apply to patients with severe hypoxaemia failing conventional ventilation, they increase uncertainty about the role of HFOV even in these patients.
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Lumb, Andrew B., and Natalie Drury. Respiratory physiology in anaesthetic practice. Edited by Jonathan G. Hardman. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0002.

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Moving away from the structure of traditional texts, this chapter follows the journey of oxygen molecules as they move from inspired air to their point of use in mitochondria, with some digressions along the way to cover other relevant aspects of respiratory physiology. The chapter encompasses all the key aspects of respiratory physiology and also highlights physiological alterations that occur under both general and regional anaesthesia, moving the physiological principles discussed into daily anaesthetic practice. The chapter explores relevant anatomy of the airways, lungs, and pleura. The histology and function of the airway lining and alveoli are described, so illustrating the importance of pulmonary defence mechanisms for protecting the internal milieu of the body from this large and fragile interface with the outside world. Key principles and concepts including resistance, compliance, and diffusion are all discussed in their clinical context. Concepts relating to the mechanics of breathing and the control of airway diameter are considered along with lung volumes and their measurement. Both the central and peripheral mechanisms involved in the control of breathing are discussed with particular attention to the impact of anaesthesia. The relationship between ventilation and perfusion and the carriage of oxygen and carbon dioxide are all discussed in detail. The principles behind key respiratory measurements such as dead space, lung volumes, diffusing capacity, and shunt are all described. Overall the chapter provides a comprehensive review of respiratory physiology as well as including additional aspects of variation that occur under anaesthesia.
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Book chapters on the topic "Alveolar mechanics"

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Romero, P. V. "Alveolar micromechanics." In Basics of Respiratory Mechanics and Artificial Ventilation, 119–31. Milano: Springer Milan, 1999. http://dx.doi.org/10.1007/978-88-470-2273-7_10.

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Albert, S., B. Kubiak, and G. Nieman. "Protective Mechanical Ventilation: Lessons Learned From Alveolar Mechanics." In Yearbook of Intensive Care and Emergency Medicine, 245–55. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-77290-3_23.

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Stenqvist, O., and H. Odenstedt. "Alveolar Pressure/volume Curves Reflect Regional Lung Mechanics." In Yearbook of Intensive Care and Emergency Medicine, 407–14. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-49433-1_37.

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Tanne, Kazuo. "Biomechanical Responses of Craniofacial and Alveolar Bones to Mechanical Forces in Orthodontics." In Interfaces in Medicine and Mechanics—2, 299–308. Dordrecht: Springer Netherlands, 1991. http://dx.doi.org/10.1007/978-94-011-3852-9_31.

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Meissner, S., L. Knels, T. Koch, E. Koch, S. Adami, X. Y. Hu, and N. A. Adams. "Experimental and Numerical Investigation on the Flow-Induced Stresses on the Alveolar-Epithelial-Surfactant-Air Interface." In Notes on Numerical Fluid Mechanics and Multidisciplinary Design, 67–80. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-20326-8_4.

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Scharnagl, Hubert, Winfried März, Markus Böhm, Thomas A. Luger, Federico Fracassi, Alessia Diana, Thomas Frieling, et al. "Alveolar Proteinosis." In Encyclopedia of Molecular Mechanisms of Disease, 69. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_6651.

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Scharnagl, Hubert, Winfried März, Markus Böhm, Thomas A. Luger, Federico Fracassi, Alessia Diana, Thomas Frieling, et al. "Alveolar Lipoproteinosis." In Encyclopedia of Molecular Mechanisms of Disease, 69. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_6652.

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Scharnagl, Hubert, Winfried März, Markus Böhm, Thomas A. Luger, Federico Fracassi, Alessia Diana, Thomas Frieling, et al. "Alveolar Phospholipidosis." In Encyclopedia of Molecular Mechanisms of Disease, 69. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_6653.

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Braun-Falco, Markus, Henry J. Mankin, Sharon L. Wenger, Markus Braun-Falco, Stephan DiSean Kendall, Gerard C. Blobe, Christoph K. Weber, et al. "Pulmonary Alveolar Phospholipoproteinosis." In Encyclopedia of Molecular Mechanisms of Disease, 1754–55. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_6655.

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Braun-Falco, Markus, Henry J. Mankin, Sharon L. Wenger, Markus Braun-Falco, Stephan DiSean Kendall, Gerard C. Blobe, Christoph K. Weber, et al. "Pulmonary Alveolar Proteinosis." In Encyclopedia of Molecular Mechanisms of Disease, 1755–56. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_1491.

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Conference papers on the topic "Alveolar mechanics"

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Dong, Jun, Huimin Lv, Yue Yang, and Yonggang Zhu. "Mixing in deformable alveolar cavity." In 22nd Australasian Fluid Mechanics Conference AFMC2020. Brisbane, Australia: The University of Queensland, 2020. http://dx.doi.org/10.14264/5c5ed86.

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Oeckler, RA, BJ Walters, RW Stroetz, and RD Hubmayr. "Osmotic Pressure Alters Alveolar Epithelial Cell Plasma Membrane Mechanics Via PIP2 and Cytoskeletal Rearrangement." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2499.

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Merrikh, A. A., and J. L. Lage. "Time-Dependent Diffusion in the Alveolar Region of the Lungs: Effect of Moving Red Blood Cells." In ASME 2002 International Mechanical Engineering Congress and Exposition. ASMEDC, 2002. http://dx.doi.org/10.1115/imece2002-39530.

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Results from a preliminary numerical simulation of alveolar gas diffusion with moving capillary red blood cells (RBCs) are presented. The alveolar region is modeled with four basic constituents, namely the alveolus (or gas region), the tissue (a region lumping the alveolar and capillary membranes, and the interstitial fluid), the blood plasma (a liquid region) and the RBCs. A single, straight capillary with equally spaced RBCs moving together with the blood plasma is considered in this preliminary study. The numerical simulation attempts also to mimic the time-varying gas concentration in the alveolus region due to respiration. Realistic physical parameters (e.g., dimensions, diffusivities and RBCs speed) are used for simulating CO diffusion, in accordance to clinical tests for determining the lung diffusing capacity. Results are compared to published results obtained when the RBCs are fix in place (stationary). The RBCs moving effect, relevant at high hematocrit, is to increase the resulting lung diffusing capacity.
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Wallbank, A. M., S. Niemiec, C. Zgheib, E. Nozik, K. Liechty, and B. J. Smith. "The Relationship Between Alveolar Leak and Lung Mechanics in Endotoxin-Induced Acute Lung Injury with CNP-miR146a Treatment." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a4659.

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Krueger, Alexander, Lilla Knels, Sven Meissner, Martina Wendel, Axel R. Heller, Thomas Lambeck, Thea Koch, and Edmund Koch. "Three-dimensional Fourier-domain optical coherence tomography of alveolar mechanics in stepwise inflated and deflated isolated and perfused rabbit lungs." In European Conference on Biomedical Optics. Washington, D.C.: OSA, 2007. http://dx.doi.org/10.1364/ecbo.2007.6627_6.

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Krueger, Alexander, Lilla Knels, Sven Meissner, Martina Wendel, Axel R. Heller, Thomas Lambeck, Thea Koch, and Edmund Koch. "Three-dimensional Fourier-domain optical coherence tomography of alveolar mechanics in stepwise inflated and deflated isolated and perfused rabbit lungs." In European Conference on Biomedical Optics, edited by Peter E. Andersen and Zhongping Chen. SPIE, 2007. http://dx.doi.org/10.1117/12.727891.

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Parameswaran, Harikrishnan, Ascanio D. Araújo, and Béla Suki. "Estimating Mechanical Forces In The Alveolar Walls." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a3653.

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Schneider, D., K. Smith, J. Speth, C. Wilke, D. Lyons, L. R. K. Penke, A. Lauring, B. B. Moore, and M. Peters-Golden. "Mechanisms of Alveolar Macrophage Derived Extracellular Vesicle Defense Against Influenza Infection of Alveolar Epithelial Cells." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a7425.

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Wall, Wolfgang A., Andrew Comerford, Lena Wiechert, and Sophie Rausch. "Coupled and Multi-Scale Building Blocks for a Comprehensive Computational Lung Model." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206407.

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Mechanical ventilation is a vital supportive therapy for critical care patients suffering from Acute Respiratory Distress syndrome (ARDS) or Acute Lung Injury (ALI) in view of oxygen supply. However, a number of associated complications often occur, which are collectively termed ventilator induced lung injuries (VILI) [1]. Biologically, these diseases manifest themselves at the alveolar level and are characterized by inflammation of the lung parenchyma following local overdistension or high shear stresses induced by frequent alveolar recruitment and derecruitment. Despite the more recent adoption of protective ventilation strategies based on the application of lower tidal volumes and a positive end-expiratory pressure (PEEP), patient mortality rates are with approximately 40% still very high. Understanding the reason why the lungs still become damaged or inflamed during mechanical ventilation is a key question sought by the medical community. In this contribution, an overview on recently developed building blocks of a comprehensive lung model will be given, with a main focus on lower airways.
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McGee, Maria, and Henry Rothberger. "MECHANISMS OF PROCOAGULANT GENERATION BY ALVEOLAR MACROPHAGES DURING MATURATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643168.

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During maturation in vivo and in vitro alveolar macrophages generate procoagulant(s) capable of activating the extrinsic pathway. It is generally agreed that at least part of the activity is due to TF (tissue factor). However, whether or not macrophages also generate functional factor VII or X is controversial. To characterize procoagulant activity increases, we measured kinetic parameters defining interactions between components of the TF-VII complex on membranes of alveolar macrophages either freshly isolated or cultured in serum free medium. In incubation mixtures with fixed concentrations of macrophages and added factor VII, the rate of factor Xa formation (measured by S-2222 hydrolysis) approached a maximum as factor X concentration was increased. Estimated concentrations of factor X yielding 1/2 maximal activation rates, (apparent Km) were 127.1±26 nM and 99.7±34 nM for fresh and cultured cells, respectively. Vmax (maximal velocities) were 1.21±0.24 and 8.9±5 nM Xa/min/106 cells. When concentrations of added factor X were kept constant, the rate of factor X activation increased as the added factor VII concentration was increased. For fresh and cultured cells, the respective apparent Kd were 1.810.7 and 1.410.25 nM. Maximal rates observed with X concentration fixed at 108 nM were 0.46±10.06 and 5.7±1.6 nM Xa/min/106 cells. In the absence of either added factor X or added factor VII, no factor Xa generation was detected in fresh or cultured cells, during 10-20 min incubation periods used for kinetic studies. The observed increase in Vmax without changes in apparent Km and Kd indicate that gains in procoagulant activity during macrophage maturation are due to increases in the number of functional binding sites for factor VII, without significant generation of functional vitamin K dependent factors (VII and X) by the cells. The data also indicate that maturation does not alter the rate behaviour of the TF-VII enzymatic complex on macrophage membranes. Mechanisms of complex assembly that we observed on macrophage membranes are similar to those described for the TF-VII complex assembly on purified systems.
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