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Hypervolemia induces and potentiates lung damage after recruitment maneuver in a model of sepsis-induced acute lung injury |
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| Authors: | Pedro L Silva Fernanda F Cruz Livia C Fujisaki Gisele P Oliveira Cynthia S Samary Debora S Ornellas Tatiana Maron-Gutierrez Nazareth N Rocha Regina Goldenberg Cristiane SNB Garcia Marcelo M Morales Vera L Capelozzi Marcelo Gama de Abreu Paolo Pelosi Patricia RM Rocco |
| Affiliation: | 1. Laboratory of Pulmonary Investigation, Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, Av. Carlos Chagas Filho, s/n, 21949-902, Rio de Janeiro, Brazil 2. Laboratory of Cellular and Molecular Physiology, Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, Av. Carlos Chagas Filho, s/n, 21949-902, Rio de Janeiro, Brazil 3. Laboratory of Cell and Molecular Cardiology, Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, Av. Carlos Chagas Filho, s/n, 21949-902, Rio de Janeiro, Brazil 4. Department of Physiology and Pharmacology, Fluminense Federal University, Rua Professor Hernani Pires de Melo 101, 24210-130, Niterói, Rio de Janeiro, Brazil 5. Department of Pathology, Faculty of Medicine, University of S?o Paulo, Dr. Arnaldo Street, 455, 01246-903, Sao Paulo, Brazil 6. Pulmonary Engineering Group, Department of Anaesthesiology and Intensive Care Therapy, University Hospital Carl Gustav Carus, Technical University of Dresden, Fetscherstr. 74, 01307, Dresden, Germany 7. Department of Ambient, Health and Safety, University of Insubria, Servizio di Anestesia B, Ospedale di Circolo e Fondazione Macchi viale Borri 57, 21100, Varese, Italy |
| Abstract: | IntroductionRecruitment maneuvers (RMs) seem to be more effective in extrapulmonary acute lung injury (ALI), caused mainly by sepsis, than in pulmonary ALI. Nevertheless, the maintenance of adequate volemic status is particularly challenging in sepsis. Since the interaction between volemic status and RMs is not well established, we investigated the effects of RMs on lung and distal organs in the presence of hypovolemia, normovolemia, and hypervolemia in a model of extrapulmonary lung injury induced by sepsis.MethodsALI was induced by cecal ligation and puncture surgery in 66 Wistar rats. After 48 h, animals were anesthetized, mechanically ventilated and randomly assigned to 3 volemic status (n = 22/group): 1) hypovolemia induced by blood drainage at mean arterial pressure (MAP)≈70 mmHg; 2) normovolemia (MAP≈100 mmHg), and 3) hypervolemia with colloid administration to achieve a MAP≈130 mmHg. In each group, animals were further randomized to be recruited (CPAP = 40 cm H2O for 40 s) or not (NR) (n = 11/group), followed by 1 h of protective mechanical ventilation. Echocardiography, arterial blood gases, static lung elastance (Est,L), histology (light and electron microscopy), lung wet-to-dry (W/D) ratio, interleukin (IL)-6, IL-1β, caspase-3, type III procollagen (PCIII), intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) mRNA expressions in lung tissue, as well as lung and distal organ epithelial cell apoptosis were analyzed.ResultsWe observed that: 1) hypervolemia increased lung W/D ratio with impairment of oxygenation and Est,L, and was associated with alveolar and endothelial cell damage and increased IL-6, VCAM-1, and ICAM-1 mRNA expressions; and 2) RM reduced alveolar collapse independent of volemic status. In hypervolemic animals, RM improved oxygenation above the levels observed with the use of positive-end expiratory pressure (PEEP), but increased lung injury and led to higher inflammatory and fibrogenetic responses.ConclusionsVolemic status should be taken into account during RMs, since in this sepsis-induced ALI model hypervolemia promoted and potentiated lung injury compared to hypo- and normovolemia. |
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