The role of thoracic trauma in inflammatory responses, apoptosis and bacterial translocation following multipl trauma

Background: Blunt chest trauma and its complications are common clinical problems in emergency medicine. We used a rat model for to investigate the evolution thoracic trauma role of inflammation, apoptosis and bacterial translocation in multiple traumas.
Materials and Methods: 90 Wistar rats were divided nine groups. Rats were performed a standardized blunt thoracic and/or head trauma and sacrified 24, 48 hours after the trauma. Multiple specimens from different organs and blood samples were collected and quantitatively cultured for aerobic organisms. Interleukins, TNF-α, MCP-1 levels were assessed in sera and apoptosis in lungs.
Results: Levels of interleukins, TNF-α and MCP-1 in all trauma groups significantly increased compared to control groups (p=0,001). Levels of apoptotic cell in head and thoracic trauma (HTT) groups significantly increased compared to respective Control group (p=0,009). Light microscopic evaluating of all groups, damage significantly increased in HTT groups compared to C group. The incidence of bacterial translocation was significantly higher in HTT group (p=0,003).
Conclusions: Multitude of inflammatory mediators is activated in multiple traumas including blunt thoracic trauma and bacterial translocation and apoptotic process to be formed. We believe plays major role of thoracic truma in post traumatic bacterial tranlocation inflammation and apoptozis after the multipl trauma.