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      Effects of sigh during pressure control and pressure support ventilation in pulmonary and extrapulmonary mild acute lung injury

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          Abstract

          Introduction

          Sigh improves oxygenation and lung mechanics during pressure control ventilation (PCV) and pressure support ventilation (PSV) in patients with acute respiratory distress syndrome. However, so far, no study has evaluated the biological impact of sigh during PCV or PSV on the lung and distal organs in experimental pulmonary (p) and extrapulmonary (exp) mild acute lung injury (ALI).

          Methods

          In 48 Wistar rats, ALI was induced by Escherichia coli lipopolysaccharide either intratracheally (ALIp) or intraperitoneally (ALIexp). After 24 hours, animals were anesthetized and mechanically ventilated with PCV or PSV with a tidal volume of 6 mL/kg, FiO 2 = 0.4, and PEEP = 5 cmH 2O for 1 hour. Both ventilator strategies were then randomly assigned to receive periodic sighs (10 sighs/hour, Sigh) or not (non-Sigh, NS). Ventilatory and mechanical parameters, arterial blood gases, lung histology, interleukin (IL)-1β, IL-6, caspase-3, and type III procollagen (PCIII) mRNA expression in lung tissue, and number of apoptotic cells in lung, liver, and kidney specimens were analyzed.

          Results

          In both ALI etiologies: (1) PCV-Sigh and PSV-Sigh reduced transpulmonary pressure, and (2) PSV-Sigh reduced the respiratory drive compared to PSV-NS. In ALIp: (1) PCV-Sigh and PSV-Sigh decreased alveolar collapse as well as IL-1β, IL-6, caspase-3, and PCIII expressions in lung tissue, (2) PCV-Sigh increased alveolar-capillary membrane and endothelial cell damage, and (3) abnormal myofibril with Z-disk edema was greater in PCV-NS than PSV-NS. In ALIexp: (1) PSV-Sigh reduced alveolar collapse, but led to damage to alveolar-capillary membrane, as well as type II epithelial and endothelial cells, (2) PCV-Sigh and PSV-Sigh increased IL-1β, IL-6, caspase-3, and PCIII expressions, and (3) PCV-Sigh increased the number of apoptotic cells in the lung compared to PCV-NS.

          Conclusions

          In these models of mild ALIp and ALIexp, sigh reduced alveolar collapse and transpulmonary pressures during both PCV and PSV; however, improved lung protection only during PSV in ALIp.

          Electronic supplementary material

          The online version of this article (doi:10.1186/s13054-014-0474-4) contains supplementary material, which is available to authorized users.

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          Most cited references29

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          An official American Thoracic Society workshop report: features and measurements of experimental acute lung injury in animals.

          Acute lung injury (ALI) is well defined in humans, but there is no agreement as to the main features of acute lung injury in animal models. A Committee was organized to determine the main features that characterize ALI in animal models and to identify the most relevant methods to assess these features. We used a Delphi approach in which a series of questionnaires were distributed to a panel of experts in experimental lung injury. The Committee concluded that the main features of experimental ALI include histological evidence of tissue injury, alteration of the alveolar capillary barrier, presence of an inflammatory response, and evidence of physiological dysfunction; they recommended that, to determine if ALI has occurred, at least three of these four main features of ALI should be present. The Committee also identified key "very relevant" and "somewhat relevant" measurements for each of the main features of ALI and recommended the use of least one "very relevant" measurement and preferably one or two additional separate measurements to determine if a main feature of ALI is present. Finally, the Committee emphasized that not all of the measurements listed can or should be performed in every study, and that measurements not included in the list are by no means "irrelevant." Our list of features and measurements of ALI is intended as a guide for investigators, and ultimately investigators should choose the particular measurements that best suit the experimental questions being addressed as well as take into consideration any unique aspects of the experimental design.
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            A simple method for assessing the validity of the esophageal balloon technique.

            The validity of the conventional esophageal balloon technique as a measure of pleural pressure was tested in 10 subjects in sitting, supine, and lateral positions by occluding the airways at end-expiration and measuring the ratio of changes in esophageal (delta Pes) and mouth pressure (delta Pm) during the ensuing spontaneous occluded inspiratory efforts. Similar measurements were also made during static Mueller maneuvers. In both tests, delta Pes/delta Pm values were close to unity in sitting and lateral positions, whereas in the supine position, substantial deviations from unity were found in some instances. However, by repositioning the balloon to different levels in the esophagus, even in these instances a locus could be found where the delta Pes/delta Pm ratio was close to unity. No appreciable phase difference between delta Pes and delta Pm was found. We conclude that by positioning the balloon according to the "occlusion test" procedure, valid measurements of pleural pressure can be obtained in all the tested body positions.
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              Regulation and repair of the alveolar-capillary barrier in acute lung injury.

              Considerable progress has been made in understanding the basic mechanisms that regulate fluid and protein exchange across the endothelial and epithelial barriers of the lung under both normal and pathological conditions. Clinically relevant lung injury occurs most commonly from severe viral and bacterial infections, aspiration syndromes, and severe shock. The mechanisms of lung injury have been identified in both experimental and clinical studies. Recovery from lung injury requires the reestablishment of an intact endothelial barrier and a functional alveolar epithelial barrier capable of secreting surfactant and removing alveolar edema fluid. Repair mechanisms include the participation of endogenous progenitor cells in strategically located niches in the lung. Novel treatment strategies include the possibility of cell-based therapy that may reduce the severity of lung injury and enhance lung repair.
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                Author and article information

                Contributors
                lillianmoraes78@gmail.com
                cintialsvet@gmail.com
                rss.quelzinha@gmail.com
                fernanda_fcruz@yahoo.com.br
                fsaddy@gmail.com
                mmorales@biof.ufrj.br
                vcapelozzi@lim05.fm.usp.br
                pedro.leme@gmail.com
                mgabreu@uniklinikum-dresden.de
                crisbaezgarcia@gmail.com
                ppelosi@hotmail.com
                prmrocco@gmail.com
                Journal
                Crit Care
                Critical Care
                BioMed Central (London )
                1364-8535
                1466-609X
                12 August 2014
                12 August 2014
                2014
                : 18
                : 4
                : 474
                Affiliations
                [ ]Laboratory of Pulmonary Investigation, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Centro de Ciências da Saúde, Avenida Carlos Chagas Filho, s/n, Bloco G-014, Ilha do Fundão, 21941-902 Rio de Janeiro, RJ Brazil
                [ ]Laboratory of Experimental Surgery, Faculty of Medicine, Federal University of Rio de Janeiro, Avenida Pedro Calmon, 550, Rio de Janeiro, RJ 21941-901 Brazil
                [ ]Hospital Pró-Cardíaco, Rua General Polidoro, 192, Rio de Janeiro, RJ 22280-003 Brazil
                [ ]Hospital Copa D’Or, Rua Figueiredo Magalhães, Rio de Janeiro, RJ 22031-011 Brazil
                [ ]Laboratory of Cellular and Molecular Physiology, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Avenida Pedro Calmon, 550, Rio de Janeiro, RJ 21941-901 Brazil
                [ ]Department of Pathology, School of Medicine, University of São Paulo, Avenida Prof. Almeida Prado, 1280, São Paulo, SP 05508-070 Brazil
                [ ]Pulmonary Engineering Group, Department of Anesthesiology and Intensive Care Therapy, University Hospital Carl Gustav Carus, Dresden University of Technology, Mommsenstraße 11, 01069 Dresden, Germany
                [ ]Rio de Janeiro Federal Institute of Education, Science and Technology, Rua Prof. Carlos Wenceslau, 343, Rio de Janeiro, RJ 25715-000 Brazil
                [ ]Department of Surgical Sciences and Integrated Diagnostics, University of Genoa, IRCCS AOU San Martino-IST, Largo Rosanna Benzi 10, I-16132 Genoa, Italy
                Article
                474
                10.1186/s13054-014-0474-4
                4155110
                25113136
                c319df12-3246-4af5-a827-9584e3c4125a
                © Moraes et al., licensee BioMed Central Ltd. 2014

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                : 14 May 2014
                : 23 July 2014
                Categories
                Research
                Custom metadata
                © The Author(s) 2014

                Emergency medicine & Trauma
                Emergency medicine & Trauma

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