Watts Ryan P, Thom Ogilvie, Fraser John F
Critical Care Research Group, The Prince Charles Hospital, Rode Road, Chermside, QLD, Australia.
J Transplant. 2013;2013:521369. doi: 10.1155/2013/521369. Epub 2013 Apr 15.
Brain death is associated with dramatic and serious pathophysiologic changes that adversely affect both the quantity and quality of organs available for transplant. To fully optimise the donor pool necessitates a more complete understanding of the underlying pathophysiology of organ dysfunction associated with transplantation. These injurious processes are initially triggered by catastrophic brain injury and are further enhanced during both brain death and graft transplantation. The activated inflammatory systems then contribute to graft dysfunction in the recipient. Inflammatory mediators drive this process in concert with the innate and adaptive immune systems. Activation of deleterious immunological pathways in organ grafts occurs, priming them for further inflammation after engraftment. Finally, posttransplantation ischaemia reperfusion injury leads to further generation of inflammatory mediators and consequent activation of the recipient's immune system. Ongoing research has identified key mediators that contribute to the inflammatory milieu inherent in brain dead organ donation. This has seen the development of novel therapies that directly target the inflammatory cascade.
脑死亡与剧烈且严重的病理生理变化相关，这些变化会对可用于移植的器官数量和质量产生不利影响。要充分优化供体库，就需要更全面地了解与移植相关的器官功能障碍的潜在病理生理学。这些损伤过程最初由灾难性脑损伤引发，并在脑死亡和器官移植过程中进一步加剧。激活的炎症系统随后会导致受体的移植物功能障碍。炎症介质与固有免疫系统和适应性免疫系统协同驱动这一过程。器官移植物中有害免疫途径被激活，使其在植入后更容易发生进一步炎症。最后，移植后缺血再灌注损伤会导致炎症介质进一步生成，并进而激活受体的免疫系统。正在进行的研究已经确定了导致脑死亡器官捐献中固有炎症环境的关键介质。这促使了直接针对炎症级联反应的新型疗法的发展。
