Plasma membrane stress failure in ventilator-injured lungs: A hypothesis about osmoregulation and the pharmacologic protection of the lungs against deformation injury

Jose L. Mendez, Otis B. Rickman, Rolf D. Hubmayr

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Cell injury and repair are invariable consequences of mechanical ventilation with large tidal volumes. Rate and amplitude of deforming stress affect numerous cell metabolic functions including host defense and wound repair. Recently, we have focused on the role of plasma membrane stress failure as a trigger for a pro-inflammatory response in mechanically ventilated lungs. We have developed both cell- and organ-based models to study this problem. Alveolar epithelial cells that are exposed to deforming stresses seek to maintain sublytic plasma membrane tension and may activate mechanisms of cell surface area regulation to control membrane tension. Interventions which either increase the amount of excess plasma membrane or enhance lipid trafficking should be cytoprotective against deformation induced injury. Osmotic manipulation may be one such intervention. Preconditioning the lungs with anisosmotic solutions may allow the cells to recruit excess plasma membrane and thus be more resistant to ventilator-induced lung injury.

Original languageEnglish (US)
Pages (from-to)290-292
Number of pages3
JournalBiology of the Neonate
Volume85
Issue number4
DOIs
StatePublished - 2004

Fingerprint

Osmoregulation
Mechanical Ventilators
Cell Membrane
Lung
Wounds and Injuries
Ventilator-Induced Lung Injury
Alveolar Epithelial Cells
Tidal Volume
Artificial Respiration
Lipids
Membranes

Keywords

  • Cell membrane
  • Lung injury
  • Mechanical stress
  • Osmolar concentration

ASJC Scopus subject areas

  • Developmental Biology
  • Pediatrics, Perinatology, and Child Health

Cite this

Plasma membrane stress failure in ventilator-injured lungs : A hypothesis about osmoregulation and the pharmacologic protection of the lungs against deformation injury. / Mendez, Jose L.; Rickman, Otis B.; Hubmayr, Rolf D.

In: Biology of the Neonate, Vol. 85, No. 4, 2004, p. 290-292.

Research output: Contribution to journalArticle

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