The basic pathogenic mechanism of the diabetic retinopathy is hyperglycaemia. Capillary damage could be explained by several mechanisms. Among many causes the sorbitol overload, the excessive storage of advanced glycosylation endproducts, oxidative stress and/or the cell apoptosis after the paradoxical glucose starvation can be emphasised. The article further analyses mechanism of capillary damage in the retina is on the basis of hemorheological, hemodynamical and histopathological changes. The specific role of the retinal pigment epithelium is described. Histopathological changes accompanying the elementary microcirculatory anomalies result from the apoptotic death of pericytes, damage of endothelial cells, and impairment of the basal membrane. Microcirculatory changes, which include the capillary dilation, vascular occlusion, and proliferation of new vessels, bring about further development of the diabetic retinopathy.

        Key words: pathophysiology, diabetic retinopathy, hyperglycaemia, pericytes, endothelial cells.