Recruitment maneuver in pulmonary and extrapulmonary experimental acute lung injury.
OBJECTIVE
The aim of this study is to test the hypothesis that recruitment maneuvers (RMs) might act differently in models of pulmonary (p) and extrapulmonary (exp) acute lung injury (ALI) with similar transpulmonary pressure changes.


METHODS
Prospective, randomized, controlled experimental study.


METHODS
University research laboratory.


METHODS
Wistar rats were randomly divided into four groups. In control groups, sterile saline solution was intratracheally (0.1 mL, Cp) or intraperitoneally (1 mL, Cexp) injected, whereas ALI animals received Escherichia coli lipopolysaccharide intratracheally (100 microg, ALIp) or intraperitoneally (1 mg, ALIexp). After 24 hrs, animals were mechanically ventilated (tidal volume, 6 mL/kg; positive end-expiratory pressure, 5 cm H2O) and three RMs (pressure inflations to 40 cm H2O for 40 secs, 1 min apart) applied.


RESULTS
PaO2, lung resistive and viscoelastic pressures, static elastance, lung histology (light and electron microscopy), and type III procollagen messenger RNA expression in pulmonary tissue were measured before RMs and at the end of 1 hr of mechanical ventilation. Mechanical variables, gas exchange, and the fraction of area of alveolar collapse were similar in both ALI groups. After RMs, lung resistive and viscoelastic pressures and static elastance decreased more in ALIexp (255%, 180%, and 118%, respectively) than in ALIp (103%, 59%, and 89%, respectively). The amount of atelectasis decreased more in ALIexp than in ALIp (from 58% to 19% and from 59% to 33%, respectively). RMs augmented type III procollagen messenger RNA expression only in the ALIp group (19%), associated with worsening in alveolar epithelium injury but no capillary endothelium lesion, whereas the ALIexp group showed a minor detachment of the alveolar capillary membrane.


CONCLUSIONS
Given the same transpulmonary pressures, RMs are more effective at opening collapsed alveoli in ALIexp than in ALIp, thus improving lung mechanics and oxygenation with limited damage to alveolar epithelium.
Riva
Douglas R
DR
Laboratory of Respiration Physiology, Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Oliveira
Mariana B G
MB
Rzezinski
Andréia F
AF
Rangel
Graziela
G
Capelozzi
Vera L
VL
Zin
Walter A
WA
Morales
Marcelo M
MM
Pelosi
Paolo
P
Rocco
Patricia R M
PR
D000403:Airway Resistance / Q000502:physiology; D000818:Animals; D002199:Capillary Permeability / Q000502:physiology; D024061:Collagen Type III / Q000235:genetics; D004195:Disease Models, Animal; D004730:Endothelium, Vascular / Q000473:pathology / Q000503:physiopathology; D015870:Gene Expression / Q000502:physiology; D008170:Lung Compliance / Q000502:physiology*; D008854:Microscopy, Electron; D010100:Oxygen / Q000097:blood*; D011650:Pulmonary Alveoli / Q000098:blood supply / Q000473:pathology / Q000503:physiopathology*; D001261:Pulmonary Atelectasis / Q000473:pathology / Q000503:physiopathology; D011659:Pulmonary Gas Exchange / Q000502:physiology; D012333:RNA, Messenger / Q000235:genetics; D051381:Rats; D017208:Rats, Wistar; D012128:Respiratory Distress Syndrome / Q000473:pathology / Q000503:physiopathology*; D015656:Respiratory Mechanics / Q000502:physiology*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D018746:Systemic Inflammatory Response Syndrome / Q000473:pathology / Q000503:physiopathology*
D024061:Collagen Type III; D012333:RNA, Messenger; D010100:Oxygen