• Erhan Ayan, Oğuz Koksel, Ayşe Polat, Lülüfer Tamer, Gülden Ersöz, Murat Demir, Hatice Yıldırım Yaroğlu, Alper Akdağ, Ali Ozdülger, and Sema Erden.
• Department of Thoracic Surgery, Mersin University Faculty of Medicine, Training and Research Hospital, Mersin, Turkey. erhanayan10@hotmail.com.
• Ulus Travma Acil Cer. 2013 Nov 1; 19 (6): 491-9.

BackgroundBlunt chest trauma and its complications are commonly encountered in emergency medicine. Herein, we used a rat model to investigate the role of thoracic trauma in inflammation, apoptosis and bacterial translocation following multiple traumas.MethodsNinety Wistar rats were divided equally into nine groups. Rats underwent a standardized blunt thoracic and/or head trauma and were sacrificed 24 or 48 hours after the trauma. Specimens from various organs and blood samples were collected and quantitatively cultured for aerobic organisms. Interleukins, TNF-α, and MCP-1 levels were assessed in the sera and markers of apoptosis were detected in the lungs.ResultsLevels of interleukins, TNF-α and MCP-1 in all of the groups undergoing trauma were significantly higher than those of the control group (p=0.001). Levels of apoptotic cells in the groups undergoing head and thoracic trauma (HTT) were significantly higher than those of the control group (p=0.009). Light microscopic evaluation indicated that damage in the HTT groups was significantly higher than that in the control group. The incidence of bacterial translocation was also significantly higher in the HTT groups (p=0.003).ConclusionMultiple inflammatory mediators are activated in multiple traumas (including blunt thoracic trauma), which allow bacterial translocation and apoptotic processes to occur. Our results indicate that thoracic trauma plays a major role in post-traumatic bacterial translocation, inflammation, and apoptosis following multiple traumas.

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