Hirntodinduzierte aktivierung proinflammatorischer reaktionen in potentiellen spenderorganen

Background: Organ dysfunction after explosive brain death has been well documented. In addition, a series of nonspecific inflammatory events may increase the intensity of the immunological host response. The aim of the present study was to monitor the course of proinflammatory cytokines in heart, lung and kidney after brain death induction. Methods: Brain death (BD) was induced in 4 pigs by inflation of an intracranial Foley catheter and separately 4 pigs were sham-operated. Each experiment was terminated 6 hours after brain death/sham operation and the organs were harvested. We determined the mRNA-expression for TNF-α, IL-1β and IL-6 in the heart, lung and kidney using rt-PCR techniques. The results are presented as absorbance intensity (Mean ± SEM). β-actin was used for standardization. Results: After 6 hours, IL-1β and IL-6 mRNA expression increased significantly in all investigated organs in the brain dead animals compared to sham-operated. TNF-α transcripts increased significantly only in lung, while in heart and kidney TNF-α mRNA tended even to lower values in brain dead animals. Conclusion: Brain death was associated with an increase in mRNA concentration of IL-1β and IL-6 in lung, heart and kidney, while TNF-α mRNA expression was only up-regulated in lung. We suggest that brain death initiates a cascade of organ-specific inflammatory events that may play a crucial role in early graft dysfunction and rejection via a priming effect on the transplanted organ.