Effect of brain death and donor treatment on organ inflammatory response and donor organ viability

Abstract
Purpose of review In the past, brain death in the donor has been recognized as an important risk factor for the success of solid organ transplantation. Brain death-related systemic changes that may influence potential donor organs do not seem to be restricted to hormonal and hemodynamic alterations. This review shows that at present there is convincing evidence for an inflammatory response in the donor organs as a direct result of brain death. This may be caused by systemic factors released from the brain as a result of its damage. Also, new research is reviewed suggesting the presence of other processes that occur at organ level in brain death. Recent findings In most organs, there is currently proof that the endothelium is activated, combined with the expression of adhesion molecules. The amount of leukocyte invasion in the tissue differs between organs. Recently, by using a microarray technique, the authors discovered the upregulation of several genes in brain death, which could be divided into three groups: genes involved in inflammation and coagulation, cell division and fibrosis, and protection and repair processes. Summary These findings in brain death of an inflammatory response at organ level together with a first attempt of the organ to protect itself offer new opportunities in donor treatment and preservation. By focusing attention on the specific blocking or stimulating of these processes, graft survival may be enhanced. The first studies in this direction already show promising results for graft survival.

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