Organ-specific regulation of pro-inflammatory molecules in heart, lung, and kidney following brain death

Background. Nonspecific inflammatory events following brain death may increase the intensity of the immunological host response. The present study investigated the course of pro-inflammatory molecules in heart, lung, kidney, and plasma after brain death induction. Materials and methods. Brain death was induced in five pigs by inflation of an intracranial Foley catheter and five pigs were sham-operated as controls. Each experiment was terminated 6 It after brain death/sham operation and the organs were harvested. We measured the mRNA and protein levels for TNF-alpha, IL-1beta, and IL-6 in heart, lung, kidney, and plasma. Additionally, the mRNA expression for IL-6R, ICAM-1, MCP-1, and TGF-beta was determined in each organ. Results. After 6 h, the plasma cytokine levels were higher in the brain-dead animals than in the shamoperated. In heart, lung, and kidney there was an increase in IL-6 and IL-1beta following brain death, while TNF-a was up-regulated in lung only (P < 0.05). MCP-1 and TGF-beta were significantly higher in heart and lung and IL-6R increased in heart after brain death (P < 0.05). Conclusions. Brain death was associated with nonuniform cytokine expression patterns in the investigated organs. These expression patterns may cause variable pro-inflammatory priming resulting in different degrees of damage and explain the organ-specific variation in outcomes after transplantations. (C) 2004 Elsevier Inc. All rights reserved.