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Plasma membrane disruptions with different modes of injurious mechanical ventilation in normal rat lungs*
Matteo Pecchiari1, Ario Monaco, Antonia Koutsoukou
1Dipartimento di Fisiologia Umana, Università degli Studi di Milano, Milan, Italy.
Objectives:
Plasma membrane disruptions are caused by excessive mechanical stress and thought to be involved in inflammatory mediator upregulation. Presently, plasma membrane disruption formation has been studied only during mechanical ventilation with large tidal volumes and limitedly to subpleural alveoli. No information is available concerning the distribution of plasma membrane disruptions within the lung or the development of plasma membrane disruptions during another modality of injurious mechanical ventilation, i.e., mechanical ventilation with eupneic tidal volume (7 mL · kg) at low end-expiratory lung volume. The aim of this study is to assess whether 1) mechanical ventilation with eupneic tidal volume at low end-expiratory lung volume causes plasma membrane disruptions; and 2) the distribution of plasma membrane disruptions differs from that of mechanical ventilation with large tidal volume at normal end-expiratory lung volume.
Design:
Experimental animal model.
Subjects:
Sprague-Dawley rats.
Interventions:
Plasma membrane disruptions have been detected as red spots in gelatin-included slices of rat lungs stained with ethidium homodimer-1 shortly after anesthesia (control) after prolonged mechanical ventilation with eupneic tidal volume at low end-expiratory lung volume followed or not by the restoration of physiological end-expiratory lung volume and after prolonged mechanical ventilation with large tidal volumes and normal end-expiratory lung volume.
Measurements And Main Results:
Plasma membrane disruptions increased during mechanical ventilation at low end-expiratory lung volume, mainly at the bronchiolar level. Resealing of most plasma membrane disruptions occurred on restoration of normal end-expiratory lung volume. Mechanical ventilation with large tidal volume caused the appearance of plasma membrane disruptions, both bronchiolar and parenchymal, the latter to a much greater extent than with mechanical ventilation at low end-expiratory lung volume. The increase of plasma membrane disruptions correlated with the concomitant increase of airway resistance with both modes of mechanical ventilation.
Conclusions:
: Amount and distribution of plasma membrane disruptions between small airways and lung parenchyma depends on the type of injurious mechanical ventilation. This could be relevant to the release of inflammatory mediators.
Insights
Mechanical ventilation can cause plasma membrane disruptions in the lungs, particularly at the bronchiolar level. The distribution and severity of these disruptions depend on the ventilation strategy, impacting airway resistance and potentially inflammatory mediator release.
Area of Science:
- Pulmonary physiology
- Cell biology
- Mechanical ventilation research
Background:
- Plasma membrane disruptions are linked to mechanical stress and inflammatory responses.
- Previous studies focused on high tidal volume ventilation and subpleural alveoli.
- The impact of eupneic tidal volume ventilation at low lung volumes on plasma membrane integrity was unknown.
Purpose of the Study:
- To investigate if mechanical ventilation with eupneic tidal volume at low end-expiratory lung volume causes plasma membrane disruptions.
- To determine if the distribution of these disruptions differs from high tidal volume ventilation.
- To assess the correlation between plasma membrane disruptions and airway resistance.
Main Methods:
- Utilized an experimental animal model with Sprague-Dawley rats.
- Detected plasma membrane disruptions using ethidium homodimer-1 staining in lung slices.
- Compared ventilation with eupneic tidal volume at low lung volumes versus large tidal volumes at normal lung volumes.
Main Results:
- Mechanical ventilation at low end-expiratory lung volume increased plasma membrane disruptions, primarily in bronchioles.
- Restoring normal lung volumes facilitated resealing of most disruptions.
- High tidal volume ventilation induced both bronchiolar and parenchymal disruptions, with greater parenchymal involvement.
- Increased plasma membrane disruptions correlated with increased airway resistance in both ventilation modes.
Conclusions:
- The type of injurious mechanical ventilation influences the amount and distribution of plasma membrane disruptions.
- These disruptions occur in small airways and lung parenchyma.
- Findings suggest a link between ventilation strategy, plasma membrane integrity, and inflammatory mediator release.
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