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Journal articles on the topic 'Alveolar recruitment'

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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 0 to 40 mmHg in 5-mmHg increments. The largest group of alveoli (42%) recruited gradually. Another group (33%) recruited suddenly (sheet flow). Half of the neighborhoods had at least one alveolus that paradoxically derecruited when pressure was increased, even though neighboring alveoli continued to recruit capillaries. At pulmonary venous pressures of 40 mmHg, 86% of the alveolar-capillary networks were not fully recruited. We conclude that the pattern of recruitment among neighboring alveoli is complex, is not homogeneous, and may not reach full recruitment, even under extreme pressures.

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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% increase in lung gas volume, the average alveolar depth decreases 21 ±5%, the average alveolar duct radius increases 7 ± 3%, and the total number of alveoli increases by 96 ± 9% (results are means ± SD between subjects; P < 0.001, P < 0.01, and P < 0.00001, respectively, via paired t-tests). Thus our results indicate that in healthy human subjects the lung inflates primarily by alveolar recruitment and, to a lesser extent, by anisotropic expansion of alveolar ducts.

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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 placed on the lung surface. The lung was recruited to three recruitment pressures (RP) of 20, 30, or 40 cmH2O for 40 s while subpleural alveoli were continuously filmed. Following measurement of microscopic alveolar recruitment, the lungs were excised, and macroscopic gross lung recruitment was digitally filmed. Recruitment was quantified by computer image analysis, and data were interpreted using a mathematical model. The majority of alveolar recruitment (78.3 ± 7.4 and 84.6 ± 5.1%) occurred in the first 2 s (T2) following application of RP 30 and 40, respectively. Only 51.9 ± 5.4% of the microscopic field was recruited by T2 with RP 20. There was limited recruitment from T2 to T40 at all RPs. The majority of gross lung recruitment also occurred by T2 with gradual recruitment to T40. The data were accurately predicted by a mathematical model incorporating the effects of both pressure and time. Alveolar recruitment is determined by the magnitude of recruiting pressure and length of time pressure is applied, a concept supported by our mathematical model. Such a temporal dependence of alveolar recruitment needs to be considered when recruitment maneuvers for clinical application are designed.

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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-volume curve during 15 min. Cardiorespiratory parameters were measured at baseline (before RM) and 1 and 4 h later. RM-induced lung recruitment was measured using the pressure-volume curve method. Net alveolar fluid clearance was measured by measuring changes in bronchoalveolar protein concentrations before and after RM. Results In responders, defined as patients showing an RM-induced increase in arterial oxygen tension of 20% of baseline value or greater, net alveolar fluid clearance (19 +/- 13%/h) and significant alveolar recruitment (113 +/- 101 ml) were observed. In nonresponders, neither net alveolar fluid clearance (-24 +/- 11%/h) nor alveolar recruitment was measured. Responders and nonresponders differed only in terms of lung morphology: Responders had a diffuse loss of aeration, whereas nonresponders had a focal loss of aeration, predominating in the lower lobes. Conclusion In the absence of alveolar recruitment and improvement in arterial oxygenation, RM decreases the rate of alveolar fluid clearance, suggesting that lung overinflation may be associated with epithelial dysfunction.

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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 resonance imaging into three groups. After anesthesia induction, in the alveolar recruitment strategy (ARS) group, an alveolar recruitment maneuver was performed by manually ventilating the lungs with a peak airway pressure of 40 cm H2O and a PEEP of 15 cm H2O for 10 breaths. PEEP was then reduced to and kept at 5 cm H2O. The continuous positive airway pressure (CPAP) group received 5 cm H2O of continuous positive airway pressure without recruitment. The zero end-expiratory pressure (ZEEP) group received neither PEEP nor the recruitment maneuver. All patients breathed spontaneously during the procedure. After cranial magnetic resonance imaging, thoracic magnetic resonance imaging was performed. Results The atelectatic volume (median, first and third standard quartiles) detected in the ZEEP group was 1.25 (0.75-4.56) cm3 in the right lung and 4.25 (3.2-13.9) cm3 in the left lung. The CPAP group had 9.5 (3.1-23.7) cm3 of collapsed lung tissue in the right lung and 8.8 (5.3-28.5) cm3 in the left lung. Only one patient in the ARS group presented an atelectasis of less than 2 cm3. An uneven distribution of the atelectasis was observed within each lung and between the right and left lungs, with a clear predominance of the left basal paradiaphragmatic regions. Conclusion Frequency of atelectasis was much less following the alveolar recruitment strategy, compared with children who did not have the maneuver performed. The mere application of 5 cm H2O of CPAP without a prior recruitment did not show the same treatment effect and showed no difference compared to the control group without PEEP.

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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. Responders were defined based on a 30% increase in oxygenation. EELV increased in responders, whereas it remained constant in non-responders. The time course was different in individual patients. In some responders, a plateau was reached as early as 2–4 h, whereas, in others, 8 h of prone positioning was not sufficient to allow complete recruitment. The increase in lung volume was associated with both an increase in arterial oxygenation and a decrease in venous admixture. Furthermore, responders had significantly lower baseline EELVs than non-responders. In conclusion, alveolar recruitment during prone positioning has been characterized as an individual time-dependent process. Its measurement might be useful to apply prone positioning more individually and might also help to identify responders.

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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; (6) with lung injury, PEEP titration; and (7) with lung injury, PEEP titration + recruitment maneuver. Acute lung injury was induced by intratracheal instillation of hydrochloric acid. PEEP titration was performed by incremental and decremental PEEP from 5 to 20 cm H2O for optimizing arterial oxygenation. Three recruitment maneuvers (pressure of 40 cm H2O maintained for 20 s) were applied to the assigned groups at each PEEP level. Proportion of lung inflammation, hemorrhage, edema, and alveolar wall disruption were recorded on each histological field. Mean alveolar area was measured in the aerated lung regions. Results Acid aspiration increased mean alveolar area and produced alveolar wall disruption, lung edema, alveolar hemorrhage, and lung inflammation. PEEP titration significantly improved arterial oxygenation but simultaneously increased lung inflammation in juxta-diaphragmatic lung regions. Recruitment maneuver during PEEP titration did not induce additional increase in lung inflammation and alveolar hyperinflation. Conclusion In a porcine model of acid aspiration-induced lung injury, PEEP titration aimed at optimizing arterial oxygenation, substantially increased lung inflammation. Recruitment maneuvers further improved arterial oxygenation without additional effects on inflammation and hyperinflation.

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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 assessed by propidium iodide (PI) exclusion in confocal images of subpleural alveoli. Cyclic inflations of normal lungs from zero end-expiratory pressure to 40 cmH2O produced VT values of 56.9 ± 3.1 ml/kg and were associated with 0.12 ± 0.12 PI-positive cells/alveolus. A preceding tracheal instillation of normal saline (3 ml) reduced VT to 49.1 ± 6 ml/kg but was associated with a significantly greater number of wounded alveolar epithelial cells (0.52 ± 0.16 cells/alveolus; P < 0.01). Mechanical ventilation of completely saline-filled lungs with saline (VT = 52 ml/kg) to pressures between 10 and 15 cmH2O was associated with the least number of wounded epithelial cells (0.02 ± 0.02 cells/alveolus; P < 0.01). In mechanically ventilated, partially saline-filled lungs, the number of wounded cells increased substantially with VT, but, once VT was accounted for, wounding was independent of maximal PTP. We found that interfacial stress associated with the generation and destruction of liquid bridges in airspaces is the primary biophysical cell injury mechanism in mechanically ventilated lungs.

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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 from airway pressure to 30 mmHg above airway pressure. Capillary recruitment always began as capillary pressure exceeded airway pressure. At low positive airway pressures, the capillaries of the excised lobes opened suddenly over a narrow pressure range. AT higher airway pressures and in the intact thorax, recruitment occurred over a wide range of capillary pressures. We conclude that capillary perfusion begins when intracapillary pressure just exceeds alveolar pressure but that further increases in capillary pressure recruit capillaries depending on tension in the alveolar wall, whether imposed by positive airway pressure or by gravity when the lung is suspended in an intact thorax.

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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 recruitment but were ventilated for 1 h under ZEEP. Lung resistive and viscoelastic pressures and static elastance were computed before and immediately after recruitment, and at the end of 1 h of ventilation. Lungs were prepared for histology. Type III procollagen (PCIII) mRNA expression in lung tissue was analyzed by RT-PCR. Lung mechanics improved after recruitment in the CTRL and ALI groups. One hour of ventilation at ZEEP increased alveolar collapse, static elastance, and lung resistive and viscoelastic pressures. Alveolar collapse was similar in ATEL and ALI, and recruitment opened the alveoli in both groups. ALI showed higher PCIII expression than ATEL or CTRL groups. One hour of ventilation at ZEEP did not increase PCIII expression but augmented it significantly in the three groups when applied after recruitment. However, PEEP ventilation after recruitment avoided any increment in PCIII expression in all groups. In conclusion, recruitment followed by ZEEP was more deleterious in ALI than in mechanical ATEL, although ZEEP alone did not elevate PCIII expression. Ventilation with 5-cmH2O PEEP prevented derecruitment and aborted the increase in PCIII expression.

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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 affect the JE/MCP-1-driven alveolar monocyte accumulation, despite the observation that rAM constitutively expressed the JE/MCP-1 receptor CCR2, as analyzed by flow cytometry and immunohistochemistry. In contrast, depletion of rAM largely suppressed alveolar cytokine release as well as neutrophil and monocyte recruitment profiles upon combined JE/MCP-1/LPS treatment. Despite this strongly attenuated alveolar inflammatory response, increased lung permeability was still observed in rAM-depleted mice undergoing JE/MCP-1/LPS challenge. Lung leakage was abrogated by codepletion of circulating neutrophils or administration of anti-CD18. Collectively, rAM are not involved in JE/MCP-1-driven alveolar monocyte recruitment in noninflamed lungs but largely contribute to the alveolar cytokine response and enhanced early neutrophil and delayed monocyte influx under inflammatory conditions (JE/MCP-1/LPS deposition). Loss of lung barrier function observed under these conditions is rAM independent but involves circulating neutrophils via β2-integrin engagement.

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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 levels. Diffusion MRI was performed to image 3He apparent diffusion coefficient (ADC) maps in the middle coronal slices of lungs ( n = 10). ADC was measured immediately before and after two recruitment maneuvers, which were separated from each other with a wait period (8–44 min). We detected a statistically significant decrease in mean ADC after each recruitment maneuver. The relative ADC change was −21.2 ± 4.1 % after the first maneuver and −9.7 ± 5.8 % after the second maneuver. A significant relative increase in mean ADC was observed over the wait period between the two recruitment maneuvers. The extent of this ADC buildup was time dependent, as it was significantly related to the duration of the wait period. The two postrecruitment ADC measurements were similar, suggesting that the lungs returned to the same state after the recruitment maneuvers were applied. No significant intrasubject differences in ADC were observed between the corresponding PEEP levels in two rats that underwent three repeat maneuvers. Airway pressure tracings were recorded in separate rats undergoing one PEEP maneuver ( n = 3) and showed a significant relative difference in peak inspiratory pressure between pre- and poststates. These observations support the hypothesis of redistribution of alveolar gas due to recruitment of collapsed alveoli in presence of atelectasis, which was also supported by the decrease in peak inspiratory pressure after recruitment maneuvers.

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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 not detected in neutrophils isolated from BAL fluid, and BAL proteins were increased in mice deficient in a key subunit of the respiratory burst apparatus, gp91phox, similar to wild-type mice. Neutrophil recruitment elicited by intratracheal instillation of the chemokines macrophage inflammatory protein-2 and keratinocyte-derived chemokine was also accompanied by accumulation of albumin, C1q, and IgM. During neutrophil recruitment to the alveolar space, epithelial permeability facilitates delivery of host defense proteins. The observed increase in epithelial permeability requires recruitment of neutrophils, but not activation of the respiratory burst, and occurs with chemokine-induced neutrophil migration independent of LPS exposure.

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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 on the ratio arterial partial pressure of O2 (PaO2)/fraction of inspired O2 (FIO2) during mechanical ventilation. The severity of lung injury in the two models was clearly different, since PaO2/FIO2 were approximately 400 mmHg in PYO- and LPS-induced injuries, respectively. Both contrast, alveolar neutrophil influx, unstimulated oxygen metabolite production, and proteinase (elastase, gelatinase B) secretions of ex vivo alveolar PMNs were not larger in the PYO model. Thus the difference in severity was not associated with variations in alveolar neutrophil recruitment or activation. Moreover, gelatinase and leukocyte elastase activities were absent in bronchoalveolar fluid, indicating effective antiproteinase defense in alveolar spaces. We conclude that alveolar neutrophils are not sufficient to create severe respiratory failure.

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

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The alveolar air-tissue interface affects the lung NMR signal, because it results in a susceptibility-induced magnetic field inhomogeneity. The air-tissue interface effect can be detected and quantified by measuring the difference signal (Δ) from a pair of NMR images obtained using temporally symmetric and asymmetric spin-echo sequences. The present study describes a multicompartment alveolar model (consisting of a collection of noninteracting spherical water shells) that simulates the behavior of Δ as a function of the level of lung inflation and can be used to predict the NMR response to various types of lung injury. The model was used to predict Δ as a function of the inflation level (with the assumption of sequential alveolar recruitment, partly parallel to distension) and to simulate pulmonary edema by deriving equations that describe Δ for a collection of spherical shells representing combinations of collapsed, flooded, and inflated alveoli. Our theoretical data were compared with those provided by other models and with experimental data obtained from the literature. Our results suggest that NMR Δ measurements can be used to study the mechanisms underlying the lung pressure-volume behavior, to characterize lung injury, and to assess the contributions of alveolar recruitment and distension to the lung volume changes in response to the application of positive airway pressure (e.g., positive end-expiratory pressure).

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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-dependent alveolar monocyte accumulation accompanied by low CCL2 levels in bronchoalveolar lavage fluid (BALF). In contrast, LPS-treated CCR2-deficient mice lacked alveolar monocyte accumulation, which was accompanied by relatively high CCL2 levels in BALF. Similarly, wild-type mice that were treated systemically with the blocking anti-CCR2 antibody MC21 completely lacked LPS-induced alveolar monocyte trafficking that was associated with high CCL2 levels in BALF. Intratracheal application of anti-CCR2 antibody MC21 to locally block CCR2 on both resident and recruited cells did not affect LPS-induced alveolar monocyte trafficking but led to significantly increased BALF CCL2 levels. Reciprocally bone marrow-transplanted, LPS-treated wild-type and CCR2-deficient mice showed a strict inverse relationship between alveolar monocyte recruitment and BALF CCL2 levels. In addition, freshly isolated human and mouse monocytes were capable of integrating CCL2 in vitro. LPS-induced alveolar monocyte accumulation is accompanied by monocytic CCR2-dependent consumption of CCL2 levels in the lung. This feedback loop may limit the intensity of monocyte recruitment to inflamed lungs and play a role in the maintenance of homeostasis.

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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, tidal volume 10 ml/kg). PaO2 measured during peumoperitoneum was higher in group P than in group C (166∓32 mmHg vs 145∓34 mmHg at 15 minutes, P=0.028, 155∓30 mmHg vs 136∓32 mmHg at 30 minutes, P=0.035). Alveolar-arterial oxygen gradient in group P increased less after gas insufflation (13∓9 to 60∓34 mmHg vs 10∓9 to 37∓31 mmHg, P=0.013). We conclude that the alveolar recruitment strategy we applied before insufflation of the peritoneal cavity may improve oxygenation during laparoscopic hysterectomy.

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

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Alveolar macrophages are specialised resident phagocytes in the alveolus, constituting the first line of immune cellular defence in the lung. As the lung microenvironment is challenged and remodelled by inhaled pathogens and air particles, so is the alveolar macrophage pool altered by signals that maintain and/or replace its composition. The signals that induce the recruitment of circulating monocytes to the injured lung, as well as their distinct gene expression profile and susceptibility to epigenetic reprogramming by the local environment remain unclear. In this review, we summarise the unique characteristics of the alveolar macrophage pool ontogeny, phenotypic heterogeneity and plasticity during homeostasis, tissue injury and normal ageing. We also discuss new evidence arising from recent studies where investigators described how the epigenetic landscape drives the specific gene expression profile of alveolar macrophages. Altogether, new analysis of macrophages by means of “omic” technologies will allow us to identify key pathways by which these cells contribute to the development and resolution of lung disease in both mice and humans.

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