Altered Profile of Circulating Endothelial-Derived Microparticles in Ventilator-Induced Lung Injury*
Autor: | Nuria E. Cabrera-Benitez, Mingyao Liu, María-Teresa Martínez-Saavedra, Carlos Rodríguez-Gallego, Ángela Ramos-Nuez, Francisco Valladares, Jesús Villar, José L Martín-Barrasa, Sonia García-Hernández, Arthur S. Slutsky, Carlos Flores, Mercedes Muros |
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Rok vydání: | 2015 |
Předmět: |
Male
Pathology medicine.medical_specialty Ventilator-Induced Lung Injury medicine.medical_treatment Inflammation Lung injury Critical Care and Intensive Care Medicine Cell-Derived Microparticles Rats Sprague-Dawley Random Allocation Tidal Volume medicine Animals Prospective Studies Cell adhesion Lung Mechanical ventilation Pulmonary Gas Exchange Cell adhesion molecule business.industry Endothelial Cells Immunohistochemistry Rats Endothelial stem cell medicine.anatomical_structure Cytokines medicine.symptom business Cell Adhesion Molecules |
Zdroj: | Critical Care Medicine. 43:e551-e559 |
ISSN: | 0090-3493 |
DOI: | 10.1097/ccm.0000000000001280 |
Popis: | Pulmonary endothelial cell injury is central to the pathophysiology of acute lung injury. Mechanical ventilation can cause endothelial disruption and injury, even in the absence of preexisting inflammation. Platelet-endothelial cell adhesion molecule-1 is a transmembrane protein connecting adjacent endothelial cells. We hypothesized that injurious mechanical ventilation will increase circulating lung endothelial-derived microparticles, defined as microparticles positive for platelet-endothelial cell adhesion molecule-1, which could serve as potential biomarkers and mediators of ventilator-induced lung injury.Prospective randomized, controlled, animal investigation.A hospital preclinical animal laboratory.Forty-eight Sprague-Dawley rats.Animals were randomly allocated to one of the three following ventilatory protocols for 4 hours: spontaneous breathing (control group), mechanical ventilation with low tidal volume (6 mL/kg), and mechanical ventilation with high tidal volume (20 mL/kg). In both mechanical ventilation groups, positive end-expiratory pressure of 2 cm H2O was applied.We analyzed histologic lung damage, gas exchange, wet-to-dry lung weight ratio, serum cytokines levels, circulating endothelial-derived microparticles, platelet-endothelial cell adhesion molecule-1 lung protein content, and immunohistochemistry. When compared with low-tidal volume mechanical ventilation, high-tidal volume ventilation increased lung edema score and caused gas-exchange deterioration. These changes were associated with a marked increased of circulating endothelial-derived microparticles and a reduction of platelet-endothelial cell adhesion molecule-1 protein levels in the high-tidal volume lungs (p0.0001).There is an endothelial-derived microparticle profile associated with disease-specific features of ventilator-induced lung injury. This profile could serve both as a biomarker of acute lung injury and, potentially, as a mediator of systemic propagation of pulmonary inflammatory response. |
Databáze: | OpenAIRE |
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