INTRODUCTION
As a result of ischemia occurring in tissues for various reasons,
cellular energy stores are emptied, and cell death occurs as a result of
the accumulation of toxic metabolites. It is necessary to provide blood
flow to ischemic tissue for both regeneration of the cell and removal of
toxic metabolites. Reperfusion injury occurs during the re-bleeding
period following the ischemia period. Free oxygen radical (ROS)
derivatives, which are rapidly formed by the presentation of molecular
oxygen into the cell, are one of the most causing factors1. Ischemia-reperfusion (I / R) damage in tissues may
be caused clinically by transplantation surgery, aortic cross clamp
applications, tourniquet application, free tissue transfers, acute
compartment syndrome, and replantation of the amputated extremity2,3. During ischemia, toxic oxygen radicals are
produced in ischemic tissue. After reperfusion, free oxygen radicals and
superoxide radicals cause endothelial damage and increased vascular
permeability. In addition, activated adhesion molecules and cytokines
also initiate the systemic inflammatory response 4.