Spontaneous resolution of pulmonary edema caused by short periods of cyclic overinflation

Dreyfuss, Didier; Soler, P; Saumon, Georges

doi:10.1152/jappl.1992.72.6.2081

Cited by 97 publications

(55 citation statements)

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“…More subtle changes in barrier properties may include increased leakiness of the tight junctions connecting alveolar epithelial cells (38,50) or changes in active transport across the alveolar epithelial barrier (46). Reversible structural and functional changes in blood-gas barrier integrity have been reported during some in situ and in vivo lung inflation studies (17,21). The results obtained from our fluorescent cell viability assay appear to represent an irreversible breakdown of cell membrane integrity.…”

Section: L1178 Deformation-induced Injury Of Alveolar Epithelial Cellsmentioning

confidence: 65%

Equibiaxial deformation-induced injury of alveolar epithelial cells in vitro

Tschumperlin

Margulies

1998

American Journal of Physiology-Lung Cellular and Molecular Phys

147

211

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Deformation of the alveolar epithelial basement membrane with lung inflation has been implicated in blood-gas barrier breakdown during the development of ventilator-induced lung injury. To determine the vulnerability of alveolar epithelial cells to deformation-induced injury, we developed a cell-stretching device that subjects cells to cyclic, equibiaxial strains. Alveolar epithelial type II cells from primary culture were tested 1 and 5 days after seeding, during which time the cells underwent major morphological and phenotypic changes. Cells were subjected to changes in surface area of 12, 24, 37, and 50%, which corresponded to lung inflation of ∼60, 80, 100, and >100% of total lung capacity. Deformation-induced injury of alveolar epithelial cells, assessed with a fluorescent cell viability assay, increased with deformation magnitude and decreased with time elapsed after seeding. In cells stretched after 1 day in culture, the percentage of dead cells after a single deformation ranged from 0.5 to 72% over the range of deformations used. In cells stretched at 5 days, the percentage of dead cells ranged from 0 to 9% when exposed to identical deformation protocols. These results suggest that morphological and phenotypic changes with time in culture fundamentally change the vulnerability of alveolar epithelial cells to deformation.

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Section: L1178 Deformation-induced Injury Of Alveolar Epithelial Cellsmentioning

confidence: 65%

Equibiaxial deformation-induced injury of alveolar epithelial cells in vitro

Tschumperlin

Margulies

1998

American Journal of Physiology-Lung Cellular and Molecular Phys

147

211

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“…Gajic and coworkers have provided direct evidence that the VILI lesion is associated with a transient loss of endothelial and/or epithelial plasma membrane integrity (23). This is in keeping with data suggesting that removal of mechanical stress causes a rapid restoration of vascular barrier function (24)(25)(26). In cell culture failure to reseal a plasma membrane break causes cell death by necrosis, whereas a wounded and resealed cell remains viable for some time (27,28).…”

mentioning

confidence: 56%

Hypercapnic Acidosis Impairs Plasma Membrane Wound Resealing in Ventilator-injured Lungs

Doerr

Gajić

Berríos

et al. 2005

Am J Respir Crit Care Med

118

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The objective of this study was to assess the effects of hypercapnic acidosis on lung cell injury and repair by confocal microscopy in a model of ventilator-induced lung injury. Three groups of normocapnic, hypocapnic, and hypercapnic rat lungs were perfused ex vivo, either during or after injurious ventilation, with a solution containing the membrane-impermeant label propidium iodide. In lungs labeled during injurious ventilation, propidium iodide fluorescence identifies all cells with plasma membrane wounds, both permanent and transient, whereas in lungs labeled after injurious ventilation propidium iodide fluorescence identifies only cells with permanent plasma membrane wounds. Hypercapnia minimized the adverse effects of high-volume ventilation on vascular barrier function, whereas hypocapnia had the opposite effect. Despite CO 2 -dependent differences in lung mechanics and edema the number of injured subpleural cells per alveolus was similar in the three groups (0.48 Ϯ 0.34 versus 0.51 Ϯ 0.19 versus 0.43 Ϯ 0.20 for hypocapnia, normocapnia, and hypercapnia, respectively). However, compared with normocapnia the probability of wound repair was significantly reduced in hypercapnic lungs (63 versus 38%; p Ͻ 0.02). This finding was subsequently confirmed in alveolar epithelial cell scratch models. The potential relevance of these observations for lung inflammation and remodeling after mechanical injury is discussed.Keywords: permissive hypercapnia; plasma membrane wounding and repair; ventilator-induced lung injury So-called lung protective mechanical ventilation strategies emphasize lung recruitment and the avoidance of large tidal volumes. Such strategies are often associated with hypercapnic acidosis. Many experts view "permissive hypercapnia" as a necessary evil of a low tidal ventilation strategy (1). Concern about detrimental effects of acidemia on renal and cardiovascular function have motivated attempts to enhance CO 2 removal by tracheal gas insufflation (2) and have led to unsubstantiated recommendations about the use of bicarbonate buffers in hypercapnic patients (3). More recent data suggest that hypercapnia may actually protect the lung from certain manifestations of ischemiareperfusion, endotoxin, and mechanical ventilation-related injury (4-9). Hypocapnia, in contrast, and correction of acidemia may be harmful (10-12). The specific mechanisms through which hypercapnia influences lung injury and vascular barrier function remain uncertain (13). CO 2 generates H ϩ ions, which react with titratable groups in certain amino acids and/or interacts directly (Received in original form September 3, 2003; accepted in final form January 21, 2005) Supported by grants from the National Institutes of Health (HL-63178), GlaxoSmithKline, and the Brewer Foundation. with free amine groups in proteins to form carbamate residues (14-16). CO 2 -dependent effects on the generation of reactive oxygen species and reactive nitrogen species as well as effects on ion channel conductivity have all been considered (17, 18).V...

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“…VILI is likely to happen when the sum of FRC and VT exceeds maximal lung volume, being approximately 50 mL/kg in infants with nondiseased lungs and approximately 20 mL/kg in infants with RDS (32). Not only the degree but also the duration of overinflation is an important factor for VILI (33) and may happen after no more than a few minutes after mechanical ventilation with VT of 10 mL/kg in premature rabbits (34) or 46 mL/kg in adult rabbits (35). Six manual inflations of 35-40 mL/kg (bagging) for resuscitation before the start of regular mechanical ventilation led to severe compromise in gas exchange, lung mechanics, and lung histology in a preterm lamb model of RDS (36).…”

Section: Discussionmentioning

confidence: 99%

Alveolar Recruitment Promotes Homogeneous Surfactant Distribution in a Piglet Model of Lung Injury

et al. 2001

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Uneven distribution of exogenous surfactant contributes to a poor clinical response in animal models of respiratory distress syndrome. Alveolar recruitment at the time of surfactant administration may lead to more homogeneous distribution within the lungs and result in a superior clinical response. To investigate the effects of three different volume recruitment maneuvers on gas exchange, lung function, and homogeneity of surfactant distribution, we studied 35 newborn piglets made surfactant deficient by repeated airway lavage with warm saline. Volume recruitment was achieved by either a temporal increase in tidal volume or an increase in end-expiratory pressure during surfactant administration, yielding an increase in dynamic compliance of the respiratory system of 77% in the first group and an increase in functional residual capacity of 108% in the second group. A third group of piglets (all n ϭ 7) received a combination of both volume recruitment maneuvers, with increases in dynamic compliance of the respiratory system of 100% and in functional residual capacity of 192%. Those animals subjected to increased tidal volume showed an improved surfactant response in terms of oxygenation, ventilation, lung volumes, lung mechanics, and homogeneity of surfactant distribution. Increased end-expiratory volume augmented the surfactant effect only to some extent. The combination of both volume recruitment maneuvers, however, needed lung volumes beyond total lung capacity (approximately 56 mL/kg), thus probably inducing early sequelae of ventilatorinduced lung injury. We conclude that volume recruitment by means of increased tidal volumes at the time of surfactant administration leads to a superior surfactant effect owing to more homogeneous surfactant distribution within a collapsed lung. Surfactant treatment has reduced mortality and morbidity in infants with RDS (1). However, detrimental factors affecting response to therapy are numerous, such as uneven distribution of exogenous surfactant, insufficient dosage, inability of exogenous surfactant to enter the metabolic pathways, inhibition of surface activity by plasma-derived proteins, or respiratory failure caused by factors other than surfactant deficiency (2).Two clinical studies (3, 4) have identified patent ductus arteriosus, gas accumulation outside the alveolar level, and pulmonary infection as the main reasons for nonresponse in neonates with RDS, leading to an increased mortality as high as 40% of affected infants. Poor response, however, is thought to be predominantly caused by uneven surfactant distribution. Animal studies have shown that the distribution of exogenous surfactant is often nonuniform, and that nonuniform distribution patterns are associated with poor clinical response (5-7).The immediate increase in FRC after surfactant administration to infants with RDS (8 -10) can be considered to be the result of two mechanisms: stabilization of previously collapsing alveoli at end-expiration, and stabilization of alveoli already being ventilated at higher e...

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Spontaneous resolution of pulmonary edema caused by short periods of cyclic overinflation

Cited by 97 publications

References 0 publications

Equibiaxial deformation-induced injury of alveolar epithelial cells in vitro

Equibiaxial deformation-induced injury of alveolar epithelial cells in vitro

Hypercapnic Acidosis Impairs Plasma Membrane Wound Resealing in Ventilator-injured Lungs

Alveolar Recruitment Promotes Homogeneous Surfactant Distribution in a Piglet Model of Lung Injury

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