The аim – determination of the importance of various intensity systemic inflammation as initial factor of atherogenesis and character of its influence upon vascular and metabolic components of atherosclerosis.
Material and methods. The work was carried out on 30 rabbits with various intensity of systemic inflammation induced by intravenous injection of lipopolysaccharide during 16 weeks. Venous blood was taken every 2 weeks to determine indices of inflammation, lipid, lipoprotein (LP) and glucose metabolism. Subcutaneous insulin test was used to determine sensitivity to insulin. Disturbances of immune status were evaluated by plasma contents of circulating immune complexes and inclusion of low and very low casino online density LP; their atherogenic modification was determined by biotesting with mouse macrophages. Activity of renin-angiotensin system (RAS) was investigated according to ACE plasma activity. The morphological analysis of the changes of aorta and peripheral arterial vessels was performed.
Results. Development of the systemic inflammation was accompanied by significant metabolic disturbances, atherogenic and immunogenic LP modification combined with traditional risk factors, such as hypercholesterolemia and hypertriglyceridemia. Modification of blood LP was the result of their oxidation and glycosylation and was promoted by activation of RAS. The extent of LP modification was increased together with intensification of inflammatory reaction but not connected to the traditional changes of their metabolism and hypercholesterolemia. Structural changes of aorta and small arterial vessels were generalized and developed both in intimal and medial layers.
Conclusion. Systemic inflammation is an independent proatherogenic factor, taking part in the development of both metabolic and vascular components. The nature of atherogenesis under systemic inflammation differs significantly from traditional. It is much less dependent on changes of LP metabolism and is determined predominantly by their modification. Vascular atherosclerotic changes under systemic inflammation are developed on the background of significant generalized damage of different caliber arterial vessels.