Brömme H J, Loertzer H, Akçetin Z
Institut für Pathophysiologie der Martin-Luther-Universität Halle-Wittenberg, Magdeburger Strasse 18, 06097 Halle/Saale.
Urologe A. 2002 Mar;41(2):159-63. doi: 10.1007/s001200100117.
The term "ischemic reperfusion injury" encompasses all toxic events in a cell that occur during ischemia and subsequent reoxygenation. These reactions have a significant effect, for example, on the rate of organ survival in kidney transplantation. Reactive oxygen intermediates (ROI) play an important role in the process of postischemic reperfusion. The basic mechanisms of generation and detoxification of ROI as well as the possibilities for their registration and quantification under conditions of ischemic reperfusion injury in the rat kidney are demonstrated in this report. A prerequisite to developing cytoprotective strategies is understanding the precise course of these mechanisms to minimize damage caused by ischemia and the subsequent reperfusion, thus retaining the organ's function to the greatest extent.
术语“缺血再灌注损伤”涵盖了细胞在缺血及随后的再氧合过程中发生的所有毒性事件。例如,这些反应对肾移植中器官存活的几率有重大影响。活性氧中间体(ROI)在缺血后再灌注过程中起重要作用。本报告展示了ROI的生成和解毒的基本机制,以及在大鼠肾脏缺血再灌注损伤条件下对其进行记录和定量的可能性。制定细胞保护策略的一个先决条件是了解这些机制的确切过程,以尽量减少缺血和随后的再灌注造成的损伤,从而最大程度地保留器官功能。