In the performed clinical and experimental investigation there were determined the significance of lipoprotein modification in atherogenesis and the mechanisms of blood atherogenicity development. The pronounced changes of total blood cholesterol and the spectrum of lipoproteins in patients with coronary atherosclerosis were not regular and were noted only in 40-55% cases. The most regular was the increasing of blood atherogenicity, reflecting the appearance of the great amount of modified lipoproteins. One of the most important modifying factors was oxidative stress induced by the activation of blood inflammatory cells. These data were confirmed in investigations on children with acute respiratory inflammatory diseases and on rabbits with the models of acute inflammation. The other important mechanism of blood atherogenicity was the increasing of blood lipoproteins enriched with triglycerides; that led to secondary monocyte activation and oxidative stress development. The usage of lipid-lowering drug lipantil in coronary patients not only decreased the amount of cholesterol and tryglicerides in blood but also lowered blood atherogenicity and suppressed the oxidative stress. Thus the results show the existence of at least two ways of atherogenic lipoprotein formation--in the course of oxidative modification and under the enrichment with tryglicerides as a result of the lipolysis disturbances with subsequent slowing of the formation and elimination of these lipoprotein remnant forms from blood.

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