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[Postischemic reperfusion injury. Biochemical and methodological principles]
H J Brömme1, H Loertzer, Z Akçetin
1Institut für Pathophysiologie der Martin-Luther-Universität Halle-Wittenberg, Magdeburger Strasse 18, 06097 Halle/Saale. h-j.broemme@medizin.uni-halle.de
Abstract:
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.