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Intensive care medicine · Mar 2012
Effects of different tidal volumes in pulmonary and extrapulmonary lung injury with or without intraabdominal hypertension.
- Paolo Pelosi, Vera L Capelozzi, Patricia R M Rocco, Tatiana Maron-Gutierrez, Johnatas D Silva, Marcelo M Morales, Lillian Moraes, Raquel S Santos, Cristiane S N B Garcia, Mariana G Oliveira, Débora S Ornellas, and Nelson Jamel.
- Laboratório de Investigação Pulmonar, Instituto de Biofísica Carlos Chagas Filho, CCS, Universidade Federal do Rio de Janeiro, Ilha do Fundão, Rio de Janeiro 21941-902, Brazil.
- Intensive Care Med. 2012 Mar 1;38(3):499-508.
PurposeWe hypothesized that: (1) intraabdominal hypertension increases pulmonary inflammatory and fibrogenic responses in acute lung injury (ALI); (2) in the presence of intraabdominal hypertension, higher tidal volume reduces lung damage in extrapulmonary ALI, but not in pulmonary ALI.MethodsWistar rats were randomly allocated to receive Escherichia coli lipopolysaccharide intratracheally (pulmonary ALI) or intraperitoneally (extrapulmonary ALI). After 24 h, animals were randomized into subgroups without or with intraabdominal hypertension (15 mmHg) and ventilated with positive end expiratory pressure = 5 cmH(2)O and tidal volume of 6 or 10 ml/kg during 1 h. Lung and chest wall mechanics, arterial blood gases, lung and distal organ histology, and interleukin (IL)-1β, IL-6, caspase-3 and type III procollagen (PCIII) mRNA expressions in lung tissue were analyzed.ResultsWith intraabdominal hypertension, (1) chest-wall static elastance increased, and PCIII, IL-1β, IL-6, and caspase-3 expressions were more pronounced than in animals with normal intraabdominal pressure in both ALI groups; (2) in extrapulmonary ALI, higher tidal volume was associated with decreased atelectasis, and lower IL-6 and caspase-3 expressions; (3) in pulmonary ALI, higher tidal volume led to higher IL-6 expression; and (4) in pulmonary ALI, liver, kidney, and villi cell apoptosis was increased, but not affected by tidal volume.ConclusionsIntraabdominal hypertension increased inflammation and fibrogenesis in the lung independent of ALI etiology. In extrapulmonary ALI associated with intraabdominal hypertension, higher tidal volume improved lung morphometry with lower inflammation in lung tissue. Conversely, in pulmonary ALI associated with intraabdominal hypertension, higher tidal volume increased IL-6 expression.
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