Background: The pathophysiology of acute lung injury is multifactorial, and the mechanisms are difficult to prove. We have devised a study of two known and standardized animal models (hemorrhagic shock [HS] and oleic acid [OA]) to more closely reproduce the pathophysiology of posttraumatic acute lung injury.
Material And Methods: Pressure-controlled HS (group HS) was performed by withdrawing blood over 15-min until mean arterial pressure reached 35 mm Hg for 90 min.