Altered alveolar mechanics in the acutely injured lung

Schiller, Henry J.; McCann, Ulysse G.; Carney, David E.; Gatto, Louis A.; Steinberg, Jay; Nieman, Gary F.

doi:10.1097/00003246-200105000-00036

Cited by 142 publications

(123 citation statements)

References 17 publications

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“…The increase in open/recruited alveoli increases the stability of the lung. From this we hypothesize that subsequent cycles would progressively increase the stability of the alveoli until eventually the majority become stable and exhibit minimal change in size during tidal breathing, as postulated by Mead and coworkers (28) and shown by Nieman and colleagues (8,(10)(11)(12)(13)(14)(15)(29)(30)(31)(32) and Escolar and coworkers (19).…”

Section: Discussionmentioning

confidence: 70%

Alveolar Dynamics during Respiration

Namati¹,

Thiesse²,

Ryk³

et al. 2008

Am J Respir Cell Mol Biol

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The change in alveolar size and number during the full breathing cycle in mammals remains unanswered, yet these descriptors are fundamental for understanding alveolar-based diseases and for improving ventilator management. Genetic and environmental mouse models are used increasingly to evaluate the evolution of disease in the peripheral lung; however, little is known regarding alveolar structure and function in the fresh, intact lung. Therefore, we have developed an optical confocal process to evaluate alveolar dynamics in the fresh intact mouse lung and as an initial experiment, have evaluated mouse alveolar dynamics during a single respiratory cycle immediately after passive lung deflation. We observe that alveoli become smaller and more numerous at the end of inspiration, and propose that this is direct evidence for alveolar recruitment in the mouse lung. The findings reported support a new hypothesis that requires recruitable secondary (daughter) alveoli to inflate via primary (mother) alveoli rather than from a conducting airway.

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Section: Discussionmentioning

confidence: 70%

Alveolar Dynamics during Respiration

Namati¹,

Thiesse²,

Ryk³

et al. 2008

Am J Respir Cell Mol Biol

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“…In the supine position, gravity causes the heart to be suspended from the sternum, occupying a larger space in the anterior compartment, whereas in the prone position, the heart is resting on the sternum, allowing more anterior lung expansion. Our EIT data set will provide a valuable comparison for future studies in subjects with lung disease or during mechanical ventilation, where alveolar recruitment and derecruitment during tidal breathing can occur [26,[28][29][30].…”

Section: Image Analysismentioning

confidence: 99%

Regional ventilation distribution in the first 6 months of life

Pham

Yuill²,

Dakin³

et al. 2010

Eur Respir J

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Electrical impedance tomography (EIT) has been used to study regional ventilation distribution in neonatal and paediatric lung disease; however, little information has been obtained in healthy newborns and infants.Data on regional ventilation distribution and regional filling characteristics were obtained using EIT in the neonatal period, at 3 and 6 months of age, in spontaneously breathing infants during non-rapid eye movement sleep. Regional ventilation distribution was described using regional end-expiratory and end-inspiratory impedance amplitudes, and geometric centre of ventilation. Regional filling characteristics were described with the phase lag or lead of the regional impedance change in comparison to global impedance change.32 infants were measured in the supine position. Regional impedance amplitudes increased with age but regional ventilation distribution remained unchanged in all infants at any age, with the dependent (posterior) lung always better ventilated. Regional filling characteristics showed that the dependent lung filled during inspiration before the nondependent lung during all followup measurements.Regional ventilation distribution and regional filling characteristics remained unchanged over the first 6 months of life, and the results obtained on regional ventilation distribution are very similar to those in adult subjects.

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“…There is a relative paucity of detailed morphometric data on injured lungs, and their interpretation is controversial (50)(51)(52)(53)(54)(55). The long-held view that the heavy injured lung collapses under its own weight has been challenged (56)(57)(58).…”

Section: Alveolar Micromechanics In Injury Statesmentioning

confidence: 99%

Cellular Stress Failure in Ventilator-injured Lungs

Vlahakis

Hubmayr

2005

Am J Respir Crit Care Med

188

120

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The clinical and experimental literature has unequivocally established that mechanical ventilation with large tidal volumes is injurious to the lung. However, uncertainty about the micromechanics of injured lungs and the numerous degrees of freedom in ventilator settings leave many unanswered questions about the biophysical determinants of lung injury. In this review we focus on experimental evidence for lung cells as injury targets and the relevance of these studies for human ventilator-associated lung injury. In vitro, the stress-induced mechanical interactions between matrix and adherent cells are important for cellular remodeling as a means for preventing compromise of cell structure and ultimately cell injury or death. In vivo, these same principles apply. Large tidal volume mechanical ventilation results in physical breaks in alveolar epithelial and endothelial plasma membrane integrity and subsequent triggering of proinflammatory signaling cascades resulting in the cytokine milieu and pathologic and physiologic findings of ventilatorassociated lung injury. Importantly, though, alveolar cells possess cellular repair and remodeling mechanisms that in addition to protecting the stressed cell provide potential molecular targets for the prevention and treatment of ventilator-associated lung injury in the future.

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Altered alveolar mechanics in the acutely injured lung

Cited by 142 publications

References 17 publications

Alveolar Dynamics during Respiration

Alveolar Dynamics during Respiration

Regional ventilation distribution in the first 6 months of life

Cellular Stress Failure in Ventilator-injured Lungs

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