Abstract
Rationale: Abnormally high stresses applied to a cell can result in the loss of cell membrane integrity and the formation of direct communications between intracellular and extracellular spaces, called plasma membrane disruptions (PMD). These lesions could be involved in the genesis of biotrauma as upregulators of proinflammatory mediators expression. Observations limited to the subpleural alveoli only indicate that PMD take place during mechanical ventilation with large tidal volumes (VT) and a normal end-expiratory lung volume (EELV). It is unknown if PMD develop during low EELV ventilation with physiological VT.
Objectives: To see if a) mechanical ventilation with physiological VT at low EELV causes PMD; and b) the parenchymal distribution of PMD differs between ventilation with large VT at normal EELV and ventilation with physiological VT at low EELV.
Methods: PMD have been detected as red spots in gelatin included slices of rat lungs stained with ethidium homodimer-1 shortly after anesthesia, after prolonged ventilation at low EELV followed or not by the restoration of physiological EELV, and after prolonged ventilation with large VT and normal EELV.
Main results: PMD increased during ventilation at low EELV, mainly at bronchiolar level. Resealing of most PMD occurred on restoration of a normal EELV. Ventilation with large VT caused the appearance of PMD both bronchiolar and parenchymal, the latter to a much greater extent than with ventilation at low EELV. The increase of PMD correlated with the concomitant increase of interrupter resistance with both modes of mechanical ventilation.
Conclusions: Entity and distribution of PMD depends on the type of injurious mechanical ventilation.
- © 2011 ERS