Liver transplantation is becoming more and more common treatment method of liver diseases. The occurring complications may result from ischemia and reperfusion. However, the precise mechanism of these changes is not fully known. Microcirculation disturbances leading to ischemic damage of cells or their death are among those factors which cause liver damage under the influence of ischemia and reperfusion. These disturbances are intensified by increase of liver ischemia time and correlate with the number of wasted away hepatocytes. Endothelial cells, Browicz-Kupffer cells, neutrophils and thrombocytes are thought to play an essential role in liver microcirculation disturbances. Disturbed balance between local vasodilators and vasoconstrictors is also an important factor as it increases the lesions caused by reperfusion due to improper blood circulation. Nitrogen oxide (NO) is the most important local vasodilator. Inhibition of its synthesis in the period of early liver damage due to reperfusion causes a decrease of blood flow and increase of the occurring changes. Such strong vasoconstrictors as endothelin-1 and thromboxane play an important role. Reperfusion by damaging endothelial cells of sinusoid vessels affects the loss of endothelial barrier by the liver sinusoid vessels.