Tissue can be paradoxically more severely damaged by reperfusion than by ischaemia itself (ischaemic-reperfu- sion injury – IRI). The mechanism of IRI has been intensively studied. Both the excessive formations of reactive oxygen radicals and calcium overload participate in the development of IRI. However, the significance of interaction between neutrophils and endothelial cells has been revealed recently. Imbalance of factors formed by endothelial cells and those formed by blood elements as well as the increased tendency to adhesion of neutrophils to the vascular endothelia during IRP has been proved. IRP effects on tissues can be pharmacologi- cally influenced by: 1. anti-oxidative therapy, 2. substitution of cytoprotective factors formed in endothelial cells and blood elements, 3. inhibition of cytotoxic factors of endothelial cells and blood elements, 4. influencing the adhesion of neutrophils to the vascular endothelia, 5. administration of drugs acting by several of the above mentioned mechanisms. However, beside the application of the anti-oxidative therapy during the organ-trans- plant operations, only few of those approaches has been used in the clinical practice.

        Key words: ischaemia, reperfusion injury, reactive oxygen species, endothelium, neutrophils, pharmacology