Generation of reactive XXXX species by a sufficient, insufficient and varicose vein wall.

@entity1 @entity66 @entity26 @entity102 @entity6312 @entity1234 @entity4096 @entity19213 @entity224 @entity1865
Despite numerous theories, the etiology and pathogenesis of primary @entity6312 remain unclear. The etiology of @entity102 ( @entity102 ) known as @entity4096 ( @entity4096 ) is related to leukocyte trapping. Leukocyte trapping involves trapping of white cells in vessel walls followed by their activation and translocation outside the vessel. Release of reactive @entity26 species (ROS) from trapped white cells has been documented. @entity224 dismutase (SOD) directly inhibits the generation of free radicals and compounds that are produced during oxidation by ROS, such as @entity1234 ( @entity1865 ). The aim of this study was to determine the involvement of free radicals in the etiology of venous changes. The following material was used for the study: fragments of @entity4096 and varices from 31 @entity1 diagnosed with chronic @entity66 in the 2nd or 3rd degree, according to clinical state, etiology, anatomy and pathophysiology (CEAP), which were qualified for surgical procedure. The levels of oxidative stress markers strongly correlated with lesions observed by USG in insufficient and @entity6312 . In both a higher concentration of @entity1865 was observed, which is a sign of lipid peroxidation. Antioxidative mechanisms, SOD activity and total antioxidative power expressed as @entity19213 were inversely proportional to @entity1865 concentration. In insufficient and @entity6312 both @entity19213 and SOD activities were significantly lower than in normal veins. The severity of clinical changes was inversely dependent on the efficiency of scavenging of ROS, which additionally proves the participation of free radicals in pathogenesis of @entity102 .
