T Kiss1, P L Silva2, R Huhle3, L Moraes2, R S Santos2, N S Felix2, C L Santos2, M M Morales4, V L Capelozzi5, M Kasper6, P Pelosi7, M Gama de Abreu3, P R M Rocco8. 1. Pulmonary Engineering Group, Department of Anesthesiology and Intensive Care Therapy, University Hospital Carl Gustav Carus, Dresden University of Technology, Dresden, Germany Laboratory of Pulmonary Investigation, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Centro de Ciências da Saúde, Rio de Janeiro, Brazil. 2. Laboratory of Pulmonary Investigation, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Centro de Ciências da Saúde, Rio de Janeiro, Brazil. 3. Pulmonary Engineering Group, Department of Anesthesiology and Intensive Care Therapy, University Hospital Carl Gustav Carus, Dresden University of Technology, Dresden, Germany. 4. Laboratory of Cellular and Molecular Physiology, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Centro de Ciências da Saúde, Rio de Janeiro, Brazil. 5. Department of Pathology, School of Medicine, University of São Paulo, São Paulo, Brazil. 6. Institute of Anatomy, University Hospital Carl Gustav Carus, Dresden University of Technology, Dresden, Germany. 7. Department of Surgical Sciences and Integrated Diagnostics, IRCCS AOU San Martino-IST, University of Genoa, Genoa, Italy. 8. Laboratory of Pulmonary Investigation, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Centro de Ciências da Saúde, Rio de Janeiro, Brazil prmrocco@gmail.com.
Abstract
BACKGROUND: Variable ventilation improves respiratory function, but it is not known whether the amount of variability in tidal volume (VT) can be reduced in recruited lungs without a deterioration of respiratory system elastance. METHODS: Acute lung inflammation was induced by intratracheal instillation of lipopolysaccharide in 35 Wistar rats. Twenty-eight animals were anaesthetized and ventilated in volume-controlled mode. Lungs were recruited by random variation of VT (mean 6 ml kg(-1), coefficient of variation 30%, normal distribution) for 30 min. Animals were randomly assigned to different amounts of VT variability (n=7 for 90 min per group): 30, 15, 7.5, or 0%. Lung function, diffuse alveolar damage, and gene expression of biological markers associated with cell mechanical stress, inflammation, and fibrogenesis were assessed. Seven animals were not ventilated and served as controls for post-mortem analyses. RESULTS: A VT variability of 30%, but not 15, 7.5, or 0%, prevented deterioration of respiratory system elastance [Mean (SD) -7.5 (8.7%), P<0.05; 21.1 (9.6%), P<0.05; 43.3 (25.9), P<0.05; and 41.2 (16.4), P<0.05, respectively]. Diffuse alveolar damage was lower with a VT variability of 30% than with 0% and without ventilation, because of reduced oedema and haemorrhage. A VT variability of 30, 15, or 7.5% reduced the gene expression of amphiregulin, cytokine-induced neutrophil chemoattractant-1, and tumour necrosis factor α compared with a VT variability of 0%. CONCLUSIONS: In this model of acute lung inflammation, a VT variability of 30%, compared with 15 and 7.5%, was necessary to avoid deterioration of respiratory system elastance and was not associated with lung histological damage.
BACKGROUND: Variable ventilation improves respiratory function, but it is not known whether the amount of variability in tidal volume (VT) can be reduced in recruited lungs without a deterioration of respiratory system elastance. METHODS:Acute lung inflammation was induced by intratracheal instillation of lipopolysaccharide in 35 Wistar rats. Twenty-eight animals were anaesthetized and ventilated in volume-controlled mode. Lungs were recruited by random variation of VT (mean 6 ml kg(-1), coefficient of variation 30%, normal distribution) for 30 min. Animals were randomly assigned to different amounts of VT variability (n=7 for 90 min per group): 30, 15, 7.5, or 0%. Lung function, diffuse alveolar damage, and gene expression of biological markers associated with cell mechanical stress, inflammation, and fibrogenesis were assessed. Seven animals were not ventilated and served as controls for post-mortem analyses. RESULTS: A VT variability of 30%, but not 15, 7.5, or 0%, prevented deterioration of respiratory system elastance [Mean (SD) -7.5 (8.7%), P<0.05; 21.1 (9.6%), P<0.05; 43.3 (25.9), P<0.05; and 41.2 (16.4), P<0.05, respectively]. Diffuse alveolar damage was lower with a VT variability of 30% than with 0% and without ventilation, because of reduced oedema and haemorrhage. A VT variability of 30, 15, or 7.5% reduced the gene expression of amphiregulin, cytokine-induced neutrophil chemoattractant-1, and tumour necrosis factor α compared with a VT variability of 0%. CONCLUSIONS: In this model of acute lung inflammation, a VT variability of 30%, compared with 15 and 7.5%, was necessary to avoid deterioration of respiratory system elastance and was not associated with lung histological damage.
Authors: Alessandra F Thompson; Lillian Moraes; Nazareth N Rocha; Marcos V S Fernandes; Mariana A Antunes; Soraia C Abreu; Cintia L Santos; Vera L Capelozzi; Cynthia S Samary; Marcelo G de Abreu; Felipe Saddy; Paolo Pelosi; Pedro L Silva; Patricia R M Rocco Journal: PLoS One Date: 2021-08-20 Impact factor: 3.240
Authors: Raquel F de Magalhães; Cynthia S Samary; Raquel S Santos; Milena V de Oliveira; Nazareth N Rocha; Cintia L Santos; Jamil Kitoko; Carlos A M Silva; Caroline L Hildebrandt; Cassiano F Goncalves-de-Albuquerque; Adriana R Silva; Hugo C Faria-Neto; Vanessa Martins; Vera L Capelozzi; Robert Huhle; Marcelo M Morales; Priscilla Olsen; Paolo Pelosi; Marcelo Gama de Abreu; Patricia R M Rocco; Pedro L Silva Journal: Respir Res Date: 2016-11-25
Authors: Caio G R S Wierzchon; Gisele Padilha; Nazareth N Rocha; Robert Huhle; Mariana S Coelho; Cintia L Santos; Raquel S Santos; Cynthia S Samary; Fernanda R G Silvino; Paolo Pelosi; Marcelo Gama de Abreu; Patricia R M Rocco; Pedro L Silva Journal: Front Physiol Date: 2017-12-18 Impact factor: 4.566
Authors: Cintia L Santos; Raquel S Santos; Lillian Moraes; Cynthia S Samary; Nathane S Felix; Johnatas D Silva; Marcelo M Morales; Robert Huhle; Marcelo G Abreu; Alberto Schanaider; Pedro L Silva; Paolo Pelosi; Patricia R M Rocco Journal: PLoS One Date: 2017-05-25 Impact factor: 3.240
Authors: Lillian Moraes; Pedro L Silva; Alessandra Thompson; Cintia L Santos; Raquel S Santos; Marcos V S Fernandes; Marcelo M Morales; Vanessa Martins; Vera L Capelozzi; Marcelo G de Abreu; Paolo Pelosi; Patricia R M Rocco Journal: Front Physiol Date: 2018-04-04 Impact factor: 4.566
Authors: Andreas Güldner; Robert Huhle; Alessandro Beda; Thomas Kiss; Thomas Bluth; Ines Rentzsch; Sarah Kerber; Nadja C Carvalho; Michael Kasper; Paolo Pelosi; Marcelo G de Abreu Journal: Front Physiol Date: 2018-07-12 Impact factor: 4.566
Authors: André Soluri-Martins; Lillian Moraes; Raquel S Santos; Cintia L Santos; Robert Huhle; Vera L Capelozzi; Paolo Pelosi; Pedro L Silva; Marcelo Gama de Abreu; Patricia R M Rocco Journal: Front Physiol Date: 2017-05-02 Impact factor: 4.566