Abstract

Abstract Background The complement system is part of the innate immunity, is activated immediately after trauma and is associated with ARDS, MOF and with death of multiply injured patients. The aim of the study was to investigate the complement activation in multiply injured pigs as well as its effects on the heart in vivo and in vitro. Moreover, the impact of reamed vs. non-reamed intramedullary nailing was examined with regard to the complement activation. Methods Male pigs received multiple trauma (blunt chest trauma, liver laceration, femur fracture, hemorrhagic shock), followed by femoral nailing with/without prior conventional reaming. Systemic complement hemolytic activity as well as the local cardiac expression of complement receptors was determined in vivo after trauma. Human cardiomyocytes were exposed to C3a or C5a and analyzed regarding calcium signaling and mitochondrial respiration. Results Systemic complement activation increased within 6h after trauma and was mediated via the classical and the alternative pathway. The expression of receptors for complement activation were altered locally in vivoin left ventricles. C3a and C5a acted detrimentally on human cardiomyocytes in vitro. Conclusion After multiple trauma, an early activation of the complement system is triggered, affecting the heart in vivo as well as in vitro, leading to complement-induced cardiac dysfunction. The intensity of complement activation after multiple trauma correlated with the invasiveness of fracture treatment. Consequently, the choice of fracture treatment might imply the clinical outcome of the critically injured patients and might be therefore crucial for their survival.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call