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The author reflects on the issues related to donation after cardiac death (DCD). It says that many centers are revisiting DCD to bridge the gap between gap between organ supply and demand. However, grafts have been subject to prolonged warm ischaemia (WI), which is why maintenance of organ has become an important factor. The author says that DCD is rapidly earning its place in everyday clinical transplantation practice, however, there are significant challenges to DCD donor management.

Abstract: Background: After kidney transplantation, a decreased graft survival is seen in grafts from brain dead donors compared to living donors, possibly related to a progressive inflammatory reaction in the graft. In this study, we focused on the effects of brain death on the inflammatory response (adhesion molecules, leukocyte infiltration, and gene expression) and stress-related heat shock proteins in the human kidney. Research outcomes and clinical donor parameters were linked to outcome data after transplantation. Methods: Human kidney biopsy specimens were obtained during organ retrieval from brain dead and living organ donor controls. On these specimens, immunohistochemistry and semiquantitative RT-PCR were performed. Regression analyses were performed connecting results to outcome data of kidney recipients. Results: In brain death, immunohistochemistry showed an increase of E-selectin and interstitial leukocyte invasion versus controls; RT-PCR showed an increase of gene expression of HO-1 and Hsp70. One and 3 years after transplantation, high ICAM and VCAM expression proved to have a negative effect on kidney function in brain dead and living kidneys, while HO-1 proved to have a strongly positive effect, but only in kidneys from living donors. Conclusions: E-selectin expression and interstitial leukocyte accumulation in brain dead donor kidneys indicate an early phase inflammatory state prior to organ retrieval. Also, brain death causes a stress-related response resulting in upregulation of potentially protective heat shock proteins. The upregulation of HO-1 is beneficial in living donor kidneys, but might be inadequate in brain death. [Copyright &y& Elsevier]

Abstract: Hypothermic machine perfusion (HMP) provides better protection against cold ischemic injury than cold storage in marginal donor kidneys. Also, in liver transplantation a switch from static cold storage to HMP could be beneficial as it would allow longer preservation times and the use of marginal donors. A critical question concerning application of HMP in liver preservation is the crucial balance between perfusion pressure and occurrence of endothelial injury. Rat livers were cold-perfused for 24 hours to study perfusion pressures for both hepatic artery and portal vein. Cold storage served as control and was compared to HMP-preserved livers using a mean arterial perfusion pressure of 25 mm Hg and a portal perfusion pressure of 4 mm Hg (25% of normothermic liver circulation) and to HMP at 50 mm Hg and 8 mm Hg perfusion, respectively (50% of normothermic liver circulation). UW solution was enriched with 14.9 μmol/L propidium iodide (PI) to stain for dead cells and with an additional 13.5 μmol/L acridine orange to stain for viable hepatocytes. A low PI-positive cell count was found using HMP at 25% of normal circulation compared to cold storage. The PI count was high for the HMP group perfused at just 50% of normal circulation compared to HMP at 25% and compared to cold storage. In summary, for liver HMP, perfusion at 25% showed complete perfusion with minimal cellular injury. HMP using perfusion pressures of 25 mm Hg for the hepatic artery and 4 mm Hg for the portal vein is feasible without induction of endothelial injury. [Copyright &y& Elsevier]

Abstract: Brain death donors are frequently used for transplantation. Previous studies showed that brain death (BD) negatively affects the immunological and inflammatory status of both liver and kidney. Objective: Therefore we studied the inflammatory and morphological changes in donor small intestine after brain death induction. Methods: BD was induced in rats by slow inflation of an epidural balloon catheter. Three groups (n = 6) were compared, 1 hour, 4 hours BD and sham operated controls. The liver was used as a reference to confirm our previous findings. Intestinal injury was determined using the Park score. Polymorphonuclear cells (PMNs) were counted in intestine and liver as a marker for inflammatory response. Real time PCR was used to demonstrate the effects of BD on ICAM-1 expression in the jejunum. Results: The morphology of the intestine was compromised after 1 and 4 hours BD. In brain dead rats, apical lifting of epithelial cells was clearly present, which resulted in higher Park scores compared to controls (P < .05). Liver morphology remained intact. In small intestine and liver an increased PMN influx in the 1 hour BD group was observed in comparison to controls. Hepatic PMN influx increased further in the 4 hours BD group (P < .05). ICAM-1 was upregulated in jejunum in both the 1 hour BD and 4 hours BD groups compared to controls (P < .05). In conclusion, the early occurrence of intestinal damage after BD induction may negatively influence transplant outcome. [Copyright &y& Elsevier]