Summary. Reperfusion of ischaemic tissue provides oxygen and substrates that are necessary for tissue recovery and concurrently removes toxic metabolites. However, reperfusion may induce various detrimental processes that may cause further tissue damage. Such deterioration of tissue function after reperfusion is defined as ischaemia-reperfusion injury. The consequences of ischemia-reperfusion injury vary from reversible cell dysfunction to local and remote tissue destruction, multiple organ failure and death. The pathogenesis of ischaemia-reperfusion injury is complex and includes excessive production of reactive oxygen species, activation of neutrophils, activation of complement, involvement of cytokines and other inflammatory mediators, vasoactive substances NO and endothelin. This review discusses the pathophysiology of ischaemia-reperfusion injury, the mechanisms of reactive oxygen species production, and the role of other factors in the pathogenesis of such injury. Several approaches and procedures used in pre-clinical and clinical studies in order to limit ischaemia-reperfusion injury are also presented.