O49 Aims: The majority of donor organs used for transplantation are derived from brain-dead donors. The unphysiological state of brain-death alters the hemodynamic and neurohormonal status of the donor resulting in changes in immunologically and inflammatorily compromised organs. Subsequently, graft survival is lower compared to living (un)related donors. Although brain death is an important variable for kidney and liver donation, no data is available for the intestine. Since intestinal transplantation is now feasible, we determined if its integrity is altered during brain death and, considering its position in normal abdominal circulation, whether the alterations are comparable to those observed in liver. Methods: A rat model for gradual onset of brain death was used by inflation of an epidural balloon catheter. During brain death normotension was maintained by infusion of a plasma expander. Three groups were compared each comprising six rats: 0 h sham operated controls, 1 h brain death and 4 h brain death. Liver and intestine were arterially flushed with saline just before harvesting of the organs. Liver morphology and inflammatory status were assessed. Inflammation was determined by counting the number of polymorphonuclear cells (PMNs). Changes in intestinal morphology were determined, using the park score. Results: Despite an intact liver morphology the number of PMNs in liver parenchyma was increased in the 1 h brain dead group 33.0 +/− 1.1 compared to the sham operated group 11.8 ± 0.4 PMNs per microscopic field. In the 4 h brain dead group the PMN count increased to 59.7 +/− 1.6 PMNs per microscopic field (P<0.001). 0 h brain death showed an intact intestinal morphology. After 1 h brain death a loss of apical villous brush border from the ileum was observed and at 4 h brain death damage to villi was aggravated, since we observed epithelial detachment and further deterioration of the villi. Conclusions: Brain death induction resulted in inflammatory changes in the liver, as measured by an increase in PMN influx in liver parenchyma. No morphological changes were observed in brain death donor livers. The intestinal integrity was, however, already compromised after 1 h brain death. The loss in intestinal integrity coincides with PMN influx in the liver, either as a secondary effect of the lost barrier function of villi, or by brain death induced changes in the immunological status of the intestine.