Citoesqueleto e mecanotransdução na fisiopatologia da lesão pulmonar induzida por ventilador

Taniguchi, Leandro Utino; Caldini, Elia Garcia; Velasco, Irineu Tadeu; Negri, Elnara M.

doi:10.1590/s1806-37132010000300015

Cited by 8 publications

(2 citation statements)

References 56 publications

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“…The exact mechanisms leading to VILI at the acinar level remain elusive, although it is generally accepted that mechanical strain due to exaggerated deformation at the cellular level can lead both to structural deterioration and inflammation of the parenchyma through mechanotransduction responses [4, 5]. In particular, high pressure and large volume excursions have been demonstrated to induce mechanical injury in the lung [1].…”

Section: Introductionmentioning

confidence: 99%

Dynamic Mechanical Interactions Between Neighboring Airspaces Determine Cyclic Opening and Closure in Injured Lung

Broche

Perchiazzi

Porra

et al. 2017

Critical Care Medicine

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Rationale Positive pressure ventilation exposes the lung to mechanical stresses that can exacerbate injury. The exact mechanism of this pathological process remains elusive. Objectives Describe Recruitment/Derecruitment (R/D) at acinar length scales over short time frames and test the hypothesis that mechanical interdependence between neighboring lung units determines the spatial and temporal distributions of R/D, using a computational model. Methods Experiments were performed in anaesthetized rabbits ventilated in Pressure Controlled mode (PCV). The lung was consecutively imaged at ~1.5 min intervals, at each Positive End-Expiratory Pressure (PEEP) of 12, 9, 6, 3 and 0 cmH2O before and after injury. The extent and spatial distribution of R/D was analyzed by subtracting subsequent images. In a realistic lung structure we implemented a mechanistic model in which each unit has individual pressures and speeds of opening and closing. Derecruited and Recruited lung fractions (Fderecruited, Frecruited) were computed based on the comparison of the aerated volumes at successive time points. Results Alternative R/D occurred in neighboring alveoli over short time scales in all tested PEEP levels and despite stable PCV. The computational model reproduced this behavior only when parenchymal interdependence between neighboring acini was accounted for. Simulations closely mimicked the experimental magnitude of Fderecruited and Frecruited when mechanical interdependence was included, while its exclusion gave Frecruited values of zero at PEEP ≥ 3 cmH2O. Conclusions These findings give further insight into the microscopic behavior of the injured lung and provide a means of testing protective-ventilation strategies to prevent R/D and subsequent lung damage.

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Section: Introductionmentioning

confidence: 99%

Dynamic Mechanical Interactions Between Neighboring Airspaces Determine Cyclic Opening and Closure in Injured Lung

Broche

Perchiazzi

Porra

et al. 2017

Critical Care Medicine

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“…i) Mechanotransduction: the conversion of physical forces on the cell membrane/receptors into promotion of intracellular signal transduction pathways leading to increased synthesis and secretion of cytokines ( 17 ). ii) Cell necrosis may result from injurious stretch, leading to secretion of preformed cytokines, which then modulate the production of more cytokines ( 18 ).…”

Section: Ventilator-induced Lung Inflammationmentioning

confidence: 99%

Pediatric acute respiratory distress syndrome - current views (Review)

Liu¹,

Wang²,

Liu³

et al. 2017

Exp Ther Med

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Acute respiratory distress syndrome (ARDS) mainly involves acute respiratory failure. In addition to this affected patients feel progressive arterial hypoxemia, dyspnea, and a marked increase in the work of breathing. The only clinical solution for the above pathological state is ventilation. Mechanical ventilation is necessary to support life in ARDs but it itself worsen lung injury and the term is known clinically as ‘ventilation induced lung injury’ (VILI). At the cellular level, respiratory epithelial cells are subjected to cyclic stretch, i.e. repeated cycles of positive and negative strain, during normal tidal ventilation. In aerated areas of diseased lungs, or even normal lungs subjected to injurious positive pressure mechanical ventilation, the cells are at risk of being over distended, and worsening injury by disrupting the alveolar epithelial barrier. Further, hypercapnic acidosis (HCA) in itself confers protection from stretch injury, potentially via a mechanisms involving inhibition of nuclear factor κB (NF-κB), a transcription factor central to inflammation, injury and repair. Mesenchymal stem cells are the latest in the field and are being investigated as a possible therapy for ARDS.

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Prevention and Amelioration of Rodent Ventilation-Induced Lung Injury with Either Prophylactic or Therapeutic feG Administration

Elder

Bersten

Saccone

et al. 2019

Lung

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Purpose Mechanical ventilation is a well-established therapy for patients with acute respiratory failure. However, up to 35% of mortality in acute respiratory distress syndrome may be attributed to ventilation-induced lung injury (VILI). We previously demonstrated the efficacy of the synthetic tripeptide feG for preventing and ameliorating acute pancreatitis-associated lung injury. However, as the mechanisms of induction of injury during mechanical ventilation may differ, we aimed to investigate the effect of feG in a rodent model of VILI, with or without secondary challenge, as a preventative treatment when administered before injury (prophylactic), or as a therapeutic treatment administered following initiation of injury (therapeutic). Methods Lung injury was assessed following prophylactic or therapeutic intratracheal feG administration in a rodent model of ventilation-induced lung injury, with or without secondary intratracheal lipopolysaccharide challenge. Results Prophylactic feG administration resulted in significant improvements in arterial blood oxygenation and respiratory mechanics, and decreased lung oedema, bronchoalveolar lavage protein concentration, histological tissue injury scores, blood vessel activation, bronchoalveolar lavage cell infiltration and lung myeloperoxidase activity in VILI, both with and without lipopolysaccharide. Therapeutic feG administration similarly ameliorated the severity of tissue damage and encouraged the resolution of injury. feG associated decreases in endothelial adhesion molecules may indicate a mechanism for these effects. Conclusions This study supports the potential for feG as a pharmacological agent in the prevention or treatment of lung injury associated with mechanical ventilation.

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Citoesqueleto e mecanotransdução na fisiopatologia da lesão pulmonar induzida por ventilador

Cited by 8 publications

References 56 publications

Dynamic Mechanical Interactions Between Neighboring Airspaces Determine Cyclic Opening and Closure in Injured Lung

Dynamic Mechanical Interactions Between Neighboring Airspaces Determine Cyclic Opening and Closure in Injured Lung

Pediatric acute respiratory distress syndrome - current views (Review)

Prevention and Amelioration of Rodent Ventilation-Induced Lung Injury with Either Prophylactic or Therapeutic feG Administration

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