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Published ahead of print on May 4, 2006, doi:10.1164/rccm.200506-1006OC

Am. J. Respir. Crit. Care Med., Volume 174, Number 3, August 2006, 279-289

A more recent version of this article appeared on August 1, 2006
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Submitted on June 30, 2005
Accepted on May 1, 2006

Atelectasis causes Alveolar Injury in Non-Atelectatic Lung Regions

Shinya Tsuchida1, Doreen Engelberts2, Vanya Peltekova2, Natalie Hopkins3, Helena Frndova4, Paul Babyn5, Colin McKerlie6, Martin Post7, Paul McLoughlin3, and Brian P Kavanagh1*

1 Lung Biology Program, Hospital for Sick Children, Toronto, Ontario, Canada; Department of Critical Care Medicine, Interdepartmental Division of Critical Care Medicine, Hospital for Sick Children, University of Toronto, Toronto, Ontario, Canada; Department of Anesthesia, University of Toronto, Toronto, Ontario, Canada, 2 Lung Biology Program, Hospital for Sick Children, Toronto, Ontario, Canada, 3 Department of Physiology, University College Dublin, Conway Institute, Dublin, Ireland, 4 Lung Biology Program, Hospital for Sick Children, Toronto, Ontario, Canada; Department of Critical Care Medicine, Interdepartmental Division of Critical Care Medicine, Hospital for Sick Children, University of Toronto, Toronto, Ontario, Canada, 5 Department of Radiology, Hospital for Sick Children, Toronto, Ontario, Canada, 6 Lung Biology Program, Hospital for Sick Children, Toronto, Ontario, Canada; Department of Laboratory Medicine, University of Toronto, Toronto, Ontario, Canada, 7 Lung Biology Program, Hospital for Sick Children, Toronto, Ontario, Canada; Department of Laboratory Medicine, University of Toronto, Toronto, Ontario, Canada; Department of Physiology, University of Toronto, Toronto, Ontario, Canada

* To whom correspondence should be addressed. E-mail: brian.kavanagh{at}sickkids.ca.

RATIONALE: Many authors have suggested that the mechanism by which atelectasis contributes to injury is through the repetitive opening and closing of distal airways in lung regions that are atelectatic. However, neither the topographic nor mechanistic relationships between atelectasis and distribution of lung injury are known. OBJECTIVES: To investigate how atelectasis contributes to ventilator-induced lung injury. METHODS: Surfactant depletion was performed in anesthetized rats that were then allocated to non-injurious or injurious ventilation for 90 minutes. MEASUREMENTS: Lung injury was quantified by gas exchange, compliance, histology, wet-to-dry weight and cytokine expression, and its distribution by histology, stereology, cytokine mRNA expression, in situ hybridization and immunohistochemistry. Functional residual capacity, percent atelectasis, and injury-induced lung water accumulation were measured using gravimetric and volumetric techniques. MAIN RESULTS: Atelectasis occurred in the dependent lung regions. Injurious ventilation was associated with alveolar and distal airway injury, while non-injurious ventilation was not. With injurious ventilation, alveolar injury (i.e. histology, myeloperoxidase protein expression, quantification and localization of cytokine mRNA expression) was maximal in non-dependent regions, whereas distal airway injury was equivalent in atelectatic and non-atelectatic regions. CONCLUSIONS: These data support the notion that lung injury associated with atelectasis involves trauma to the distal airways. We provide topographic and biochemical evidence that such distal airway injury is not localized solely to atelectatic areas, but is instead generalized in both atelectatic and non-atelectatic lung regions. In contrast, alveolar injury associated with atelectasis does not occur in those areas that are atelectatic, but occurs instead in remote non-atelectatic alveoli.
Key words: Atelectasis, Ventilator-Induced Lung Injury, Mechanical Ventilation




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