الفهرس 
Introduction and aim of workOnly 14 pages are availabe for public view
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Abstract
Ischemia/reperfusion injury belongs to the main reasons for inflammatory reactions in solid organ allografts with profound influence on acute as well as long-term graft function. This is mediated by a number of cytokines/chemokines, and other proinflammatory compounds which can be specifically blocked resulting in a profound reduction of I/R injury,IRI is manifested by many clinical manifestation as heamodynamic unstability ,renal dysfunction ,arrhythmia ,neurological manifestation as confulsion and other manifestation. The onset of reperfusion injury is heralded by the unclamping of the portal vein and IVC, with reperfusion of the new liver, The major anaesthetic issue during this phase is that of the so called “post reperfusion syndrome.” The hallmarkof the post reperfusion syndrome (PRS) is systemic hypotension with or without pulmonary hypertension occurring within the first 5 minutes after reperfusion of the graft. Other circulatory disturbances include bradycardia, ventricular dysrhythmias, and cardiac arrest. These changes are provoked by the rapid infusion of metabolites from the transplanted liver, which is high in potassium . We can detect ischemic reperfusion injury Immediately after reperfusion by left ventricular function may be impaired and pulmonary capillary wedge pressure, central venous pressure (CVP), and PAP usually increase with a reduction in SVR, The anesthesiologist must prepare the patient for reperfusion by many techniques as Normalize arterial blood gas tensions, Normalize serum electrolytes, Achieve body temperature >35.5±36.0 °C, Emergency drugs prepared and Blood prepared for transfusions. IRI cannot be prevented but can be attenuated by many techniques as ischemic preconditing ,antioxidant, antileakocyte.