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  • Poster presentation
  • Open Access

Effect of sustained inflation recruitment maneuvers on lung endothelial and alveolar epithelial injury in experimental acute lung injury

  • 1,
  • 1,
  • 1,
  • 1,
  • 1 and
  • 1
Critical Care20048 (Suppl 1) :P23

  • Published:


  • Recruitment Maneuver
  • Extravascular Lung Water
  • Protective Ventilation
  • Lung Injury Severity
  • Protective Ventilation Strategy
Lung volume recruitment maneuvers (RMs) are a potential adjunct to protective ventilation for acure respiratory distress syndrome patients. However, data demonstrating improvement in important outcomes such as lung injury severity and mortality are lacking. We hypothesized that RMs reduce lung endothelial and alveolar epithelial injury in a clinically relevant rat model of acid-induced lung injury. Compared with a protective ventilation strategy without RMs, sustained inflation RMs (30 cmH2O) every 30 min significantly improved oxygenation, lung volume, dead space fraction, and compliance. RMs reduced extravascular lung water (P < 0.05). RMs also reduced lung endothelial protein permeability (217 ± 28 vs 314 ± 70 extravascular plasma equivalents, P < 0.05). However, RMs did not prevent alveolar epithelial injury. Epithelial permeability and BAL RTI40 levels, a previously validated and specific marker of type I cell injury, were similar with or without RMs. RMs also decreased epithelial fluid transport, a functional marker of epithelial injury (Fig. 1; *P < 0.05 vs no injury, P < 0.05 vs no RM). There was a trend toward lower systemic blood pressure and cardiac output in the group receiving RMs. RMs did not reduce markers of airspace inflammation. In conclusion, frequent RMs improved gas exchange, and reduced lung water in part through effects on hemodynamics. RMs may protect the lung endothelium, but do not reduce alveolar epithelial injury. Because alveolar epithelial injury is associated with lung injury severity and mortality, these data suggest that RMs may not improve these patient outcomes.

Figure 1

Authors’ Affiliations

Cardiovascular Research Institute, San Francisco, California, USA


© BioMed Central Ltd. 2004