Early increase of serum angiopoietin-2 are associated with early progression to death in experimental injury.

Abstract Severe trauma induces systemic inflammatory response syndrome (SIRS) through the release of proinflammatory mediators. Angiopoietin-2 (Ang-2) is over-produced in sepsis and leads to dysfunction of endothelial cells and subsequent multiple organ dysfunction. In order to define the role of Ang-2 in lethal injury, 45 rabbits were studied; eight were administered anesthesia; 11 were sham-operated and 26 were subject to femoral injury. Concentrations of Ang-2, malondialdehyde (MDA), tumor necrosis factor-alpha (TNFα) and endotoxins (LPS) were determined in serum and of Ang-2 in tissues; vital signs and overall survival were recorded. Bacterial growth was quantitatively assessed in liver, spleen and lung of animal that died. Survival of injured animals was shorter than sham operated ones. Serum concentrations of Ang-2 at 4 h was greater among animals where death supervened early, i.e. within 48 h after injury than among rabbits that died later. That was also the case for systolic, diastolic and mean arterial pressures. Serum MDA and TNFα and tissue bacterial growth did not differ between rabbits that died early and rabbits that died late. Serum LPS remained below the limit of detection. These results suggest that circulating Ang-2 participates in the pathogenesis of SIRS after injury connected with early haemodynamic instability.