Hepatic IL-8 release during graft procurement is associated with impaired graft function after human liver...

In experimental models, brain death induces inflammatory cascades, leading to reduced graft survival. Thus far, factors prior to graft preservation have gained less attention in clinical setting. We studied pre-preservation inflammatory response and its effects on graft function in 30 brain dead liver donors and the respective recipients. Before donor graft perfusion, portal and hepatic venous blood samples were drawn for phagocyte adhesion molecule expression and plasma cytokine determinations. Donor intensive care unit stay correlated with donor C-reactive protein (R = 0.472, p = 0.013) and IL-6 (R = 0.419, p = 0.026) levels, and donor (R = 0.478, p = 0.016) and recipient gamma-glutamyl transferase (R = 0.432, p = 0.019) levels. During graft procurement, hepatic IL-8 release was observed in 17/30 donors. Grafts with hepatic IL-8 release exhibited subsequently higher alkaline phosphatase [319 (213-405) IU/L vs. 175 (149-208) IU/L, p = 0.006] and bilirubin [101 (44-139) micromol/L vs. 30 (23-72) micromol/L, p = 0.029] levels after transplantation. Our findings support the concept that inflammatory response in the brain dead organ donor contributes to the development of graft injury in human liver transplantation.