Effects of pressure support ventilation on ventilator-induced lung injury in mild acute respiratory distress syndrome depend on level of positive end-expiratory pressure: A randomised animal study.

Autor:	Magalhães PAF; From the Laboratory of Pulmonary Investigation, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Rio de Janeiro (PAFM, GAP, LM, CLS, LAM, CLB, PRMR, PLS), Graduate Program in Maternal and Child Health, Professor Fernando Figueira Institute of Comprehensive Medicine, Recife, Pernambuco (PAFM, MCMBD, LBA), Faculty of Medicine, Laboratory of Experimental Surgery, Federal University of Rio de Janeiro, Rio de Janeiro (CLS, AS), Department of Pathology, School of Medicine, University of São Paulo, São Paulo, Brazil (VLC), Department of Anesthesiology and Intensive Care Therapy, Pulmonary Engineering Group, University Hospital Carl Gustav Carus (RH, MGA), Dresden University of Technology, Dresden, Germany (RH, MGA) and Department of Surgical Sciences and Integrated Diagnostics, IRCCS AOU San Martino-IST, University of Genoa, Genoa, Italy (PP)., Padilha GA, Moraes L, Santos CL, Maia LA, Braga CL, Duarte MDCMB, Andrade LB, Schanaider A, Capellozzi VL, Huhle R, Gama de Abreu M, Pelosi P, Rocco PRM, Silva PL
Jazyk:	angličtina
Zdroj:	European journal of anaesthesiology [Eur J Anaesthesiol] 2018 Apr; Vol. 35 (4), pp. 298-306.
DOI:	10.1097/EJA.0000000000000763
Abstrakt:	Background: Harmful effects of spontaneous breathing have been shown in experimental severe acute respiratory distress syndrome (ARDS). However, in the clinical setting, spontaneous respiration has been indicated only in mild ARDS. To date, no study has compared the effects of spontaneous assisted breathing with those of fully controlled mechanical ventilation at different levels of positive end-expiratory pressure (PEEP) on lung injury in ARDS. Objective: To compare the effects of assisted pressure support ventilation (PSV) with pressure-controlled ventilation (PCV) on lung function, histology and biological markers at two different PEEP levels in mild ARDS in rats. Design: Randomised controlled experimental study. Setting: Basic science laboratory. Participants: Thirty-five Wistar rats (weight ± SD, 310 ± 19) g received Escherichia coli lipopolysaccharide (LPS) intratracheally. After 24 h, the animals were anaesthetised and randomly allocated to either PCV (n=14) or PSV (n=14) groups. Each group was further assigned to PEEP = 2 cmH2O or PEEP = 5 cmH2O. Tidal volume was kept constant (≈6 ml kg). Additional nonventilated animals (n=7) were used as a control for postmortem analysis. Main Outcome Measures: Ventilatory and mechanical parameters, arterial blood gases, diffuse alveolar damage score, epithelial integrity measured by E-cadherin tissue expression, and biological markers associated with inflammation (IL-6 and cytokine-induced neutrophil chemoattractant, CINC-1) and type II epithelial cell damage (surfactant protein-B) were evaluated. Results: In both PCV and PSV, peak transpulmonary pressure was lower, whereas E-cadherin tissue expression, which is related to epithelial integrity, was higher at PEEP = 5 cmH2O than at PEEP = 2 cmH2O. In PSV, PEEP = 5 cmH2O compared with PEEP = 2 cmH2O was associated with significantly reduced diffuse alveolar damage score [median (interquartile range), 11 (8.5 to 13.5) vs. 23 (19 to 26), P = 0.005] and expressions of IL-6 and CINC-1 (P = 0.02 for both), whereas surfactant protein-B mRNA expression increased (P = 0.03). These changes suggested less type II epithelial cell damage at a PEEP of 5 cmH2O. Peak transpulmonary pressure correlated positively with IL-6 [Spearman's rho (ρ) = 0.62, P = 0.0007] and CINC-1 expressions (ρ = 0.50, P = 0.01) and negatively with E-cadherin expression (ρ = -0.67, P = 0.0002). Conclusion: During PSV, PEEP of 5 cmH2O, but not a PEEP of 2 cmH2O, reduced lung damage and inflammatory markers while maintaining epithelial cell integrity.
Databáze:	MEDLINE
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