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Journal articles on the topic 'Alveolar recruitment'

Author: Grafiati

Published: 4 June 2021

Last updated: 5 February 2022

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1

Baumgartner, William A., Eric M. Jaryszak, Amanda J. Peterson, Robert G. Presson, and Wiltz W. Wagner. "Heterogeneous capillary recruitment among adjoining alveoli." Journal of Applied Physiology 95, no. 2 (August 2003): 469–76. http://dx.doi.org/10.1152/japplphysiol.01115.2002.

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Pulmonary capillaries recruit when microvascular pressure is raised. The details of the relationship between recruitment and pressure, however, are controversial. There are data supporting 1) gradual homogeneous recruitment, 2) sudden and complete recruitment, and 3) heterogeneous recruitment. The present study was designed to determine whether alveolar capillary networks recruit in a variety of ways or whether one model predominates. In isolated, pump-perfused canine lung lobes, fields of six neighboring alveoli were recorded with video microscopy as pulmonary venous pressure was raised from

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2

Slutsky, A. S. "Barotrauma and alveolar recruitment." Intensive Care Medicine 19, no. 7 (July 1993): 369–71. http://dx.doi.org/10.1007/bf01724874.

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3

Hajari, A. J., D. A. Yablonskiy, A. L. Sukstanskii, J. D. Quirk, M. S. Conradi, and J. C. Woods. "Morphometric changes in the human pulmonary acinus during inflation." Journal of Applied Physiology 112, no. 6 (March 15, 2012): 937–43. http://dx.doi.org/10.1152/japplphysiol.00768.2011.

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Despite decades of research into the mechanisms of lung inflation and deflation, there is little consensus about whether lung inflation occurs due to the recruitment of new alveoli or by changes in the size and/or shape of alveoli and alveolar ducts. In this study we use in vivo 3He lung morphometry via MRI to measure the average alveolar depth and alveolar duct radius at three levels of inspiration in five healthy human subjects and calculate the average alveolar volume, surface area, and the total number of alveoli at each level of inflation. Our results indicate that during a 143 ± 18% incr

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4

Albert, Scott P., Joseph DiRocco, Gilman B. Allen, Jason H. T. Bates, Ryan Lafollette, Brian D. Kubiak, John Fischer, Sean Maroney, and Gary F. Nieman. "The role of time and pressure on alveolar recruitment." Journal of Applied Physiology 106, no. 3 (March 2009): 757–65. http://dx.doi.org/10.1152/japplphysiol.90735.2008.

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Inappropriate mechanical ventilation in patients with acute respiratory distress syndrome can lead to ventilator-induced lung injury (VILI) and increase the morbidity and mortality. Reopening collapsed lung units may significantly reduce VILI, but the mechanisms governing lung recruitment are unclear. We thus investigated the dynamics of lung recruitment at the alveolar level. Rats ( n = 6) were anesthetized and mechanically ventilated. The lungs were then lavaged with saline to simulate acute respiratory distress syndrome (ARDS). A left thoracotomy was performed, and an in vivo microscope was

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5

Ghadiali, Samir N. "Making “time” for alveolar recruitment." Journal of Applied Physiology 106, no. 3 (March 2009): 751–52. http://dx.doi.org/10.1152/japplphysiol.91652.2008.

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6

Cereda, Maurizio, and Yi Xin. "Alveolar Recruitment and Lung Injury." Critical Care Medicine 41, no. 12 (December 2013): 2837–38. http://dx.doi.org/10.1097/ccm.0b013e31829cb083.

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7

Kacmarek, Robert M. "Strategies to optimize alveolar recruitment." Current Opinion in Critical Care 7, no. 1 (February 2001): 15–20. http://dx.doi.org/10.1097/00075198-200102000-00003.

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8

Mancebo, J. "PEEP, ARDS, and alveolar recruitment." Intensive Care Medicine 18, no. 7 (July 1992): 383–85. http://dx.doi.org/10.1007/bf01694337.

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9

Lista, G., F. Castoldi, F. Cavigioli, S. Bianchi, and P. Fontana. "Alveolar recruitment in the delivery room." Journal of Maternal-Fetal & Neonatal Medicine 25, sup1 (March 5, 2012): 39–40. http://dx.doi.org/10.3109/14767058.2012.663164.

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10

Esquinas, Antonio M., and Luca S. De Santo. "Alveolar recruitment manoeuvres after cardiac surgery." European Journal of Anaesthesiology 35, no. 1 (January 2018): 61–62. http://dx.doi.org/10.1097/eja.0000000000000652.

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11

Lafarge, AL, CK Kerneis, F. Scalbert, LL Larnier, AB Brusset, PE Estagnasie, and PS Squara. "Systematic alveolar recruitment after cardiac surgery." Critical Care 19, Suppl 1 (2015): P271. http://dx.doi.org/10.1186/cc14351.

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12

Kim, Jin Kyoung. "Importance of alveolar recruitment strategy revisited." Korean Journal of Anesthesiology 67, no. 2 (2014): 75. http://dx.doi.org/10.4097/kjae.2014.67.2.75.

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13

Mols, G., H. J. Priebe, and J. Guttmann. "Alveolar recruitment in acute lung injury." British Journal of Anaesthesia 96, no. 2 (February 2006): 156–66. http://dx.doi.org/10.1093/bja/aei299.

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14

Li, Guohui, and Xueyin Shi. "Alveolar Recruitment Strategies After Cardiac Surgery." JAMA 318, no. 7 (August 15, 2017): 667. http://dx.doi.org/10.1001/jama.2017.8689.

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15

Patel, Jayshil J., and Kurt Pfeifer. "Alveolar Recruitment Strategies After Cardiac Surgery." JAMA 318, no. 7 (August 15, 2017): 667. http://dx.doi.org/10.1001/jama.2017.8693.

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16

Constantin, Jean-Michel, Sophie Cayot-Constantin, Laurence Roszyk, Emmanuel Futier, Vincent Sapin, Bernard Dastugue, Jean-Etienne Bazin, and Jean-Jacques Rouby. "Response to Recruitment Maneuver Influences Net Alveolar Fluid Clearance in Acute Respiratory Distress Syndrome." Anesthesiology 106, no. 5 (May 1, 2007): 944–51. http://dx.doi.org/10.1097/01.anes.0000265153.17062.64.

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Background Alveolar fluid clearance is impaired in the majority of patients with acute respiratory distress syndrome (ARDS). Experimental studies have shown that a reduction of tidal volume increases alveolar fluid clearance. This study was aimed at assessing the impact of the response to a recruitment maneuver (RM) on net alveolar fluid clearance. Methods In 15 patients with ARDS, pulmonary edema fluid and plasma protein concentrations were measured before and after an RM, consisting of a positive end-expiratory pressure maintained 10 cm H2O above the lower inflection point of the pressure-vo

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17

Tusman, Gerardo, Stephan H. Böhm, Alejandro Tempra, Fernando Melkun, Eduardo García, Elsio Turchetto, Paul G. H. Mulder, and Burkhard Lachmann. "Effects of Recruitment Maneuver on Atelectasis in Anesthetized Children." Anesthesiology 98, no. 1 (January 1, 2003): 14–22. http://dx.doi.org/10.1097/00000542-200301000-00006.

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Background General anesthesia is known to promote atelectasis formation. High inspiratory pressures are required to reexpand healthy but collapsed alveoli. However, in the absence of positive end-expiratory pressure (PEEP), reexpanded alveoli collapse again. Using magnetic resonance imaging, the impact of an alveolar recruitment strategy on the amount and distribution of atelectasis was tested. Methods The authors prospectively randomized 24 children who met American Society of Anesthesiologists physical status I or II criteria, were aged 6 months-6 yr, and were undergoing cranial magnetic res

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18

Algaba, Á., and N. Nin. "Alveolar recruitment maneuvers in respiratory distress syndrome." Medicina Intensiva (English Edition) 37, no. 5 (June 2013): 355–62. http://dx.doi.org/10.1016/j.medine.2013.01.006.

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19

Rama-Maceiras, Pablo. "Peri-Operative Atelectasis and Alveolar Recruitment Manoeuvres." Archivos de Bronconeumología (English Edition) 46, no. 6 (June 2010): 317–24. http://dx.doi.org/10.1016/s1579-2129(10)70074-4.

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20

Reutershan, Jörg, Andre Schmitt, Klaus Dietz, Klaus Unertl, and Reinhold Fretschner. "Alveolar recruitment during prone position: time matters." Clinical Science 110, no. 6 (May 15, 2006): 655–63. http://dx.doi.org/10.1042/cs20050337.

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Alveolar recruitment is one of the beneficial effects of prone positioning in patients with ARDS (acute respiratory distress syndrome). However, responses vary among patients and, therefore, we hypothesized that alveolar recruitment is an individual time-dependent process and its measurement might be helpful to ‘dose’ prone positioning individually. In 13 patients diagnosed with ARDS, EELV (end-expiratory lung volume) was measured in the supine position, immediately after turning to the prone position, at 1, 2, 4 and 8 h in the prone position and after returning to the supine position. Respond

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21

RICHARD, JEAN-CHRISTOPHE, SALVATORE M MAGGIORE, BJORN JONSON, JORDI MANCEBO, FRANCOIS LEMAIRE, and LAURENT BROCHARD. "Influence of Tidal Volume on Alveolar Recruitment." American Journal of Respiratory and Critical Care Medicine 163, no. 7 (June 2001): 1609–13. http://dx.doi.org/10.1164/ajrccm.163.7.2004215.

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22

Unzueta, C., G. Tusman, F. Suarex-Sipmann, S. Öhm, and V. Moral. "Alveolar Recruitment Improves Ventilation During Thoracic Surgery." Survey of Anesthesiology 56, no. 6 (December 2012): 270–71. http://dx.doi.org/10.1097/01.sa.0000422675.28228.44.

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23

Amato, Marcelo B. P., Marcia S. Volpe, and Ludhmila A. Hajjar. "Alveolar Recruitment Strategies After Cardiac Surgery—Reply." JAMA 318, no. 7 (August 15, 2017): 668. http://dx.doi.org/10.1001/jama.2017.8697.

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24

Dueck, Ron. "Alveolar recruitment versus hyperinflation: a balancing act." Current Opinion in Anaesthesiology 19, no. 6 (December 2006): 650–54. http://dx.doi.org/10.1097/aco.0b013e328011015d.

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25

Zhao, Z., J. Guttmann, and K. Möller. "Mechanical ventilation with different alveolar pressures improves alveolar recruitment: a model study." Critical Care 14, Suppl 1 (2010): P187. http://dx.doi.org/10.1186/cc8419.

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26

Ambrosio, Aline M., Rubin Luo, Denise T. Fantoni, Claudia Gutierres, Qin Lu, Wen-Jie Gu, Denise A. Otsuki, Luiz M. S. Malbouisson, Jose O. C. Auler, and Jean-Jacques Rouby. "Effects of Positive End-expiratory Pressure Titration and Recruitment Maneuver on Lung Inflammation and Hyperinflation in Experimental Acid Aspiration–induced Lung Injury." Anesthesiology 117, no. 6 (December 1, 2012): 1322–34. http://dx.doi.org/10.1097/aln.0b013e31827542aa.

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Background In acute lung injury positive end-expiratory pressure (PEEP) and recruitment maneuver are proposed to optimize arterial oxygenation. The aim of the study was to evaluate the impact of such a strategy on lung histological inflammation and hyperinflation in pigs with acid aspiration-induced lung injury. Methods Forty-seven pigs were randomly allocated in seven groups: (1) controls spontaneously breathing; (2) without lung injury, PEEP 5 cm H2O; (3) without lung injury, PEEP titration; (4) without lung injury, PEEP titration + recruitment maneuver; (5) with lung injury, PEEP 5 cm H2O;

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27

Hussein, Omar, Bruce Walters, Randolph Stroetz, Paul Valencia, Deborah McCall, and Rolf D. Hubmayr. "Biophysical determinants of alveolar epithelial plasma membrane wounding associated with mechanical ventilation." American Journal of Physiology-Lung Cellular and Molecular Physiology 305, no. 7 (October 1, 2013): L478—L484. http://dx.doi.org/10.1152/ajplung.00437.2012.

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Mechanical ventilation may cause harm by straining lungs at a time they are particularly prone to injury from deforming stress. The objective of this study was to define the relative contributions of alveolar overdistension and cyclic recruitment and “collapse” of unstable lung units to membrane wounding of alveolar epithelial cells. We measured the interactive effects of tidal volume (VT), transpulmonary pressure (PTP), and of airspace liquid on the number of alveolar epithelial cells with plasma membrane wounds in ex vivo mechanically ventilated rat lungs. Plasma membrane integrity was asses

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28

Godbey, P. S., J. A. Graham, R. G. Presson, W. W. Wagner, and T. C. Lloyd. "Effect of capillary pressure and lung distension on capillary recruitment." Journal of Applied Physiology 79, no. 4 (October 1, 1995): 1142–47. http://dx.doi.org/10.1152/jappl.1995.79.4.1142.

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To investigate the effect of capillary pressure and alveolar distension on capillary recruitment, we used video-microscopy to quantify capillary recruitment in individual subpleural alveolar walls. Canine lobes were perfused with autologous blood either while inflated by positive airway pressure or while inflated by negative intrapleural pressure in the intact thorax with airway pressure remaining atmospheric. Low flow rates minimized the arteriovenous pressure gradient (< 5 mmHg), permitting capillary pressure estimation by averaging these pressures. Capillary pressure was varied stepwise

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29

MII, Seiji. "Alveolar Recruitment and Open Lung Approach : Clinical Implementation." JOURNAL OF JAPAN SOCIETY FOR CLINICAL ANESTHESIA 32, no. 2 (2012): 207–13. http://dx.doi.org/10.2199/jjsca.32.207.

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30

Arun Babu, T. "Alveolar recruitment maneuvers in ventilated children: Caution required." Indian Journal of Critical Care Medicine 15, no. 2 (2011): 141. http://dx.doi.org/10.4103/0972-5229.83005.

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31

Farias, Luciana L., Débora S. Faffe, Débora G. Xisto, Maria Cristina E. Santana, Roberta Lassance, Luiz Felipe M. Prota, Marcelo B. Amato, Marcelo M. Morales, Walter A. Zin, and Patricia R. M. Rocco. "Positive end-expiratory pressure prevents lung mechanical stress caused by recruitment/derecruitment." Journal of Applied Physiology 98, no. 1 (January 2005): 53–61. http://dx.doi.org/10.1152/japplphysiol.00118.2004.

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This study tests the hypotheses that a recruitment maneuver per se yields and/or intensifies lung mechanical stress. Recruitment maneuver was applied to a model of paraquat-induced acute lung injury (ALI) and to healthy rats with (ATEL) or without (CTRL) previous atelectasis. Recruitment was done by using 40-cmH2O continuous positive airway pressure for 40 s. Rats were, then, ventilated for 1 h at zero end-expiratory pressure (ZEEP) or positive end-expiratory pressure (PEEP; 5 cmH2O). Atelectasis was generated by inflating a sphygmomanometer around the thorax. Additional groups did not undergo

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32

Maus, Ulrich a., M. Audrey Koay, Tim Delbeck, Matthias Mack, Monika Ermert, Leander Ermert, Timothy S. Blackwell, et al. "Role of resident alveolar macrophages in leukocyte traffic into the alveolar air space of intact mice." American Journal of Physiology-Lung Cellular and Molecular Physiology 282, no. 6 (June 1, 2002): L1245—L1252. http://dx.doi.org/10.1152/ajplung.00453.2001.

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

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33

Cereda, Maurizio, Kiarash Emami, Stephen Kadlecek, Yi Xin, Puttisarn Mongkolwisetwara, Harrilla Profka, Amy Barulic, et al. "Quantitative imaging of alveolar recruitment with hyperpolarized gas MRI during mechanical ventilation." Journal of Applied Physiology 110, no. 2 (February 2011): 499–511. http://dx.doi.org/10.1152/japplphysiol.00841.2010.

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The aim of this study was to assess the utility of 3He MRI to noninvasively probe the effects of positive end-expiratory pressure (PEEP) maneuvers on alveolar recruitment and atelectasis buildup in mechanically ventilated animals. Sprague-Dawley rats ( n = 13) were anesthetized, intubated, and ventilated in the supine position (4He-to-O2 ratio: 4:1; tidal volume: 10 ml/kg, 60 breaths/min, and inspiration-to-expiration ratio: 1:2). Recruitment maneuvers consisted of either a stepwise increase of PEEP to 9 cmH2O and back to zero end-expiratory pressure or alternating between these two PEEP level

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34

Kantrow, Stephen P., Zhiwei Shen, Tonya Jagneaux, Ping Zhang, and Steve Nelson. "Neutrophil-mediated lung permeability and host defense proteins." American Journal of Physiology-Lung Cellular and Molecular Physiology 297, no. 4 (October 2009): L738—L745. http://dx.doi.org/10.1152/ajplung.00045.2009.

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Neutrophil recruitment to the alveolar space is associated with increased epithelial permeability. The present study investigated in mice whether neutrophil recruitment to the lung leads to accumulation of plasma-derived host defense proteins in the alveolar space and whether respiratory burst contributes to this increase in permeability. Albumin, complement C1q, and IgM were increased in bronchoalveolar lavage (BAL) fluid 6 h after intratracheal LPS challenge. Neutrophil depletion before LPS treatment completely prevented this increase in BAL fluid protein concentration. Respiratory burst was

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35

Delclaux, C., S. Rezaiguia-Delclaux, C. Delacourt, C. Brun-Buisson, C. Lafuma, and A. Harf. "Alveolar neutrophils in endotoxin-induced and bacteria-induced acute lung injury in rats." American Journal of Physiology-Lung Cellular and Molecular Physiology 273, no. 1 (July 1, 1997): L104—L112. http://dx.doi.org/10.1152/ajplung.1997.273.1.l104.

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Polymorphonuclear neutrophils (PMNs) are thought to play a major role in the pathogenesis of adult respiratory distress syndrome. Because the alveolar epithelium is a decisive factor in alveolo-capillary wall permeability, a toxic effect of emigrated PMNs in alveolar spaces is conceivable. We evaluated alveolar PMN function in two rat models of acute lung injury induced by alveolar instillation of endotoxin [lipopolysaccharide (LPS)] or live Pseudomonas aeruginosa (PYO). Alveolar PMNs were isolated from bronchoalveolar lavage fluid 4 and 24 h after the challenge. Hypoxemia was assessed based o

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36

Rühl, Nina, Elena Lopez-Rodriguez, Karolin Albert, Bradford J. Smith, Timothy E. Weaver, Matthias Ochs, and Lars Knudsen. "Surfactant Protein B Deficiency Induced High Surface Tension: Relationship between Alveolar Micromechanics, Alveolar Fluid Properties and Alveolar Epithelial Cell Injury." International Journal of Molecular Sciences 20, no. 17 (August 30, 2019): 4243. http://dx.doi.org/10.3390/ijms20174243.

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

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37

Durney, Carl H., Antonio G. Cutillo, and David C. Ailion. "Magnetic resonance behavior of normal and diseased lungs: spherical shell model simulations." Journal of Applied Physiology 88, no. 4 (April 1, 2000): 1155–66. http://dx.doi.org/10.1152/jappl.2000.88.4.1155.

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

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38

Maus, Ulrich A., Sandra Wellmann, Christine Hampl, William A. Kuziel, Mrigank Srivastava, Matthias Mack, M. Brett Everhart, et al. "CCR2-positive monocytes recruited to inflamed lungs downregulate local CCL2 chemokine levels." American Journal of Physiology-Lung Cellular and Molecular Physiology 288, no. 2 (February 2005): L350—L358. http://dx.doi.org/10.1152/ajplung.00061.2004.

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The CC chemokine ligand-2 (CCL2) and its receptor CCR2 are essential for monocyte trafficking under inflammatory conditions. However, the mechanisms that determine the intensity and duration of alveolar monocyte accumulation in response to CCL2 gradients in inflamed lungs have not been resolved. To determine the potential role of CCR2-expressing monocytes in regulating alveolar CCL2 levels, we compared leukocyte recruitment kinetics and alveolar CCL2 levels in wild-type and CCR2-deficient mice in response to intratracheal LPS challenge. In wild-type mice, LPS elicited a dose- and time-dependen

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39

Park, H. P., J. W. Hwang, Y. B. Kim, Y. T. Jeon, S. H. Park, M. J. Yun, and S. H. Do. "Effect of Pre-emptive Alveolar Recruitment Strategy before Pneumoperitoneum on Arterial Oxygenation during Laparoscopic Hysterectomy." Anaesthesia and Intensive Care 37, no. 4 (July 2009): 593–97. http://dx.doi.org/10.1177/0310057x0903700419.

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In a randomised, controlled, single-blind trial, we examined the effect of a pre-emptive alveolar recruitment strategy on arterial oxygenation during subsequent pneumoperitoneum. After intubation, 50 patients were randomly allocated to receive either tidal volume 10 ml/kg with no positive end-expiratory pressure (group C) or alveolar recruitment strategy of 10 manual breaths with peak inspiratory pressure of 40 cmH2O plus positive end-expiratory pressure of 15 cmH2O before gas insufflation (group P). During pneumoperitoneum, group P was ventilated with the same setting as group C (FiO2=0.35, t

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40

Şentürk, Mert, and Mehmet Tuğrul. "Alveolar recruitment during one-lung ventilation—really “one” lung?" Annals of Thoracic Surgery 75, no. 2 (February 2003): 635. http://dx.doi.org/10.1016/s0003-4975(02)04274-1.

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41

Claxton, B. A., P. Morgan, H. Mckeague, A. Mulpur, and J. Berridge. "Alveolar recruitment strategy improves arterial oxygenation after cardiopulmonary bypass." Anaesthesia 58, no. 2 (February 2003): 111–16. http://dx.doi.org/10.1046/j.1365-2044.2003.02892.x.

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42

Kleinsasser, A. "Alveolar recruitment strategy improves arterial oxygenation after cardiopulmonary bypass." Anaesthesia 58, no. 8 (July 14, 2003): 809. http://dx.doi.org/10.1046/j.1365-2044.2003.03295_9.x.

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43

&NA;. "Alveolar Recruitment and Arterial Desflurane Concentration During Bariatric Surgery." Survey of Anesthesiology 53, no. 5 (October 2009): 204–5. http://dx.doi.org/10.1097/01.sa.0000358591.03199.81.

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44

Tibério, Iolanda F. L. C., Edna A. Leick-Maldonado, Leika Miyahara, David I. Kasahara, Graziela M. G. T. Spilborghs, Milton A. Martins, and Paulo H. N. Saldiva. "EFFECTS OF NEUROKININS ON AIRWAY AND ALVEOLAR EOSINOPHIL RECRUITMENT." Experimental Lung Research 29, no. 3 (January 2003): 165–77. http://dx.doi.org/10.1080/01902140303772.

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45

Schranz, Christoph, Paul D. Docherty, Yeong Shiong Chiew, Knut Möller, and J. Geoffrey Chase. "Identifiability Analysis of a Pressure-Depending Alveolar Recruitment Model." IFAC Proceedings Volumes 45, no. 18 (2012): 137–42. http://dx.doi.org/10.3182/20120829-3-hu-2029.00015.

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46

TUSMAN, G., S. H. BÖHM, G. F. VAZQUEZ DE ANDA, J. L. DO CAMPO, and B. LACHMANN. "“Alveolar Recruitment Strategy” Improves Arterial Oxygenation During General Anaesthesia." Survey of Anesthesiology 44, no. 1 (February 2000): 56–57. http://dx.doi.org/10.1097/00132586-200002000-00058.

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47

Tusman, G., S. H. Böhm, G. F. Vazquez de Anda, J. L. do Campo, and B. Lachmann. "‘Alveolar recruitment strategy’ improves arterial oxygenation during general anaesthesia." British Journal of Anaesthesia 82, no. 1 (January 1999): 8–13. http://dx.doi.org/10.1093/bja/82.1.8.

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48

Sprung, Juraj, Francis X. Whalen, Thomas Comfere, Zeljko J. Bosnjak, Zeljko Bajzer, Ognjen Gajic, Michael G. Sarr, et al. "Alveolar Recruitment and Arterial Desflurane Concentration During Bariatric Surgery." Anesthesia & Analgesia 108, no. 1 (January 2009): 120–27. http://dx.doi.org/10.1213/ane.0b013e31818db6c7.

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49

Graf, Jerónimo. "Bedside lung volume measurement for estimation of alveolar recruitment." Intensive Care Medicine 38, no. 3 (February 7, 2012): 523–24. http://dx.doi.org/10.1007/s00134-012-2465-8.

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50

Morales-Nebreda, Luisa, Alexander V. Misharin, Harris Perlman, and G. R. Scott Budinger. "The heterogeneity of lung macrophages in the susceptibility to disease." European Respiratory Review 24, no. 137 (August 31, 2015): 505–9. http://dx.doi.org/10.1183/16000617.0031-2015.

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

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