Background: To study the changes in protein composition of atherosclerotic plaques at different stages of their development in coronary atherosclerosis using proteomics. Methods: The object of research consisted of homogenates of atherosclerotic plaques from coronary arteries at different stages of development, obtained from 15 patients. Plaque proteins were separated by two-dimensional electrophoresis. The resultant protein spots were identified by the matrix-assisted laser desorption ionization method with peptide mass mapping. Results: Groups of differentially expressed proteins, in which the amounts of proteins differed more than twofold (p < 0.05), were identified in pools of homogenates of atherosclerotic plaques at three stages of development. The amounts of the following proteins were increased in stable atherosclerotic plaques at the stage of lipidosis and fibrosis: vimentin, tropomyosin β-chain, actin, keratin, tubulin β-chain, microfibril-associated glycoprotein 4, serum amyloid P-component, and annexin 5. In plaques at the stage of fibrosis and calcification, the amounts of mimecan and fibrinogen were increased. In unstable atherosclerotic plaque of the necrotic–dystrophic type, the amounts of human serum albumin, mimecan, fibrinogen, serum amyloid P-component and annexin were increased. Conclusion: This proteomic study identifies the proteins present in atherosclerotic plaques of coronary arteries by comparing their proteomes at three different stages of plaque development during coronary atherosclerosis.

After in vitro ischemia, the content of adenosine triphosphate in myocardial bioptates from patients with heart diseases is reduced. This reduction is more pronounced in patients with coronary heart disease than in patients with rhythm disturbances. Administration of the antioxidant preparation histochrome to patients with coronary heart disease preserves ATP during ischemic exposure. Key Words: myocardium; ischemia; ATP; lipid peroxidation; antioxidantsSurgery, a radical treatment of coronary insufficiency in coronary heart disease (CHD), is associated with risk of some grave complications, especially in early postoperation period [1]. Apart from operation wound, these complications can be caused by reperfusion damage to the myocardium [8]. A prospective way of preventing this damage is the use of antioxidant preparations [5,9]. However, recent in vitro experiments have shown that ischemia-and reperfusioninduced disturbances of myocardial contractility, in particular, myocardial contracture are due not only to altered permeability of cell membranes, but also depend on the ATP pool remaining in cardiomyocytes (CMC) before reperfusion [12]. In light of this is was interesting to evaluate the effect of acute ischemia during heart surgery and antioxidant therapy on myocardial ATP content in CHD patients. MATERIALS AND METHODSExperiments were carried out on fragments from right auricle obtained during aortocoronary bypass The fragments were washed from blood with cooled physiological saline and cut into 2 portions: one was immediately frozen in liquid nitrogen, while the other was placed to a humidified chamber (20~ for 60 rain and then frozen in liquid nitrogen. The latter procedure adequately reproduces the conditions of aortocoronary bypass operation.Some patients with CHD (n=9) were prepared for operation according to routine scheme, while others (n=8) additionally received two intravenous injections of 3% histochrome (HC) in a dose of 1 mg/kg (24 h prior to operation and in the operating room). Histochrome, a novel Russian-manufactured antioxidant, was kindly provided by Dr. A. V. Lebedev (Russian Research and Manufacturing Cardio, logy Association). Fragments obtained from patients without CHD and operated for cardiac rhythm disturbances (n=6) served as the control.

geatly intensified. The dynamics of the number of large, medium, and small lymphocytes suggests a probable change in the rate of cell dffferer tiation.Changes in the organization of the Ca+-transporting systems but not disturbances in the contractile apparatus of cardiomyocytes are shown to occur in chronic coronary heart disease. During a certain stage of CHD the change in rhythmoinotropic relations may reflect adaptive changes induced by functioning of the myocardium under conditions of ischemia.