It has been proved that the short- and long-term results of deceased donor organ transplantation are significantly worse to those obtained when the transplanted organ is obtained from a living donor. These two types of organ transplants differ by the extent of ischemia. Ischemia and accompanying proinflammatory changes have been an inevitable part of deceased donor organ procurement and transplantation and are as important factor as the immune response which influence both an early and long term function of the organ after transplantation. It occurs in several stages of the process. First begins after the brain death which is associated with hemodynamic and neuroendocrine storm, proinflammatory cytokines upregulation, nitric oxide production, oxidative stress - free radical and lipid peroxide generation, and complement activation Hypothermic storage of the kidney and preservation variables extends the injury. Reperfusion of the organ after transplantation leads to additional injury by production of oxygen free radicals. In addition during reperfusion circulating leukocytes, monocytes, and neutrophils engage strong chemoattractant gradients directing leukocyte infiltration and activation. This proinflammatory changes contribute to further endothelial and parenchymal cell death and causing microcirculatory flow disturbances.
Complete prevention of ischemia and I/R related changes is impossible. Cytoprotection in the transplanted organ may include several factors such as prevention of oxidative stress, maintenance of microcirculatyion and the use of anti-inflammatory agents. Several strategies are proposed: ischemic preconditiong, improvement of storage methods, the use of antioxidants ameliorating oxidative stress or medications preventing the mircocirculatory changes in the immediate reperfusion (ATG), or prevention of delayed graft function by other means. The proinflammatory changes associated with brain death, and the use of continuous hypothermic pulsatile perfusion will be presented.