Development of a standardized trauma-related lung injury model.

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.Pressure-controlled HS (group HS) was performed by withdrawing blood over 15-min until mean arterial pressure reached 35 mm Hg for 90 min. In an additional group, HS and standardized lung injury induced by OA were combined (group lung injury [HS + OA]). After the shock period, both groups were resuscitated over 15 min by transfusion of the removed blood and an equal volume of lactate Ringer solution. The end point was 6 h. Plasma interleukin (IL)-6, keratinocyte chemoattractant (KC), IL-10, monocyte chemoattractant protein-1 (MCP-1), and lung histology were carried out.The posttraumatic lung injury group demonstrated significantly higher IL-6 levels when compared with HS group (744.8 ± 104 versus 297.7 ± 134 pg/mL; P = 0.004). Histologic analysis confirmed diffuse alveolar congestion and moderate-to-severe lung edema in animals with HS + OA. Lung injury was mild in mice with isolated HS or OA injection.We established a posttraumatic lung injury model combining two different standardized protocols (HS and OA). This model leads to pronounced inflammation and lung injury. This model allows the analysis of the dynamics of sterile lung injury and associated organ dysfunction.