Biomedical subjects
Publications and source records attributed to A K Tikhaze.
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One-month therapy with trimetazidine sharply decreased the content of free radical oxidation products, lipid peroxides and malonic dialdehyde, in atherogenic low-density lipoproteins in patients with coronary heart disease. Activity of glutathione peroxidase utilizing lipid peroxides in the plasma markedly increased during trimetazidine therapy. The data suggest that trimetazidine not directly interacting with free radicals attenuates the adverse effects of intensive free radical oxidation in coronary heart disease. This effect is mediated via activation of antioxidant enzymes, which diminishes negative consequences of ischemia.
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Two series of studies were made to assess probucol medicines (lipomal, "Alkaloid"; fenbutol "Akrikhin") effect on clinical symptoms, lipid metabolism, primary and secondary products of lipid peroxidation, activity of antioxidant enzymes (superoxide dismutase, glutathione peroxidase) in atherosclerotic patients with hyperlipidemia type IIA and IIB. In both series probucol reduced frequency of anginal attacks, content of total cholesterol and LDL cholesterol. HDL cholesterol remained unchanged or reduced insignificantly. Lipoperoxides and malonic dialdehyde levels in plasma progressively lowered against activation of antioxidant enzymes. These biochemical parameters returned to initial values within 3 months since the drug discontinuation. It is evident that antiatherogenic effect of probucol is due to indirect activation of natural defense systems responsible for enzymic detoxication of active oxygen forms and lipoperoxides rather than to direct interaction of this synthetic antioxidant with lipid radicals.
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The authors present results of 6-month probucol (lipomal) therapy in patients with coronary heart disease concurrent with Types 2a and 2b hyperlipidemia. There were 22 and 23% increases in total cholesterol and low density lipoprotein cholesterol, respectively, whereas the levels of high density lipoprotein decreased and triglycerides remained unchanged. Having antioxidative properties, probucol enhanced the activity of the antioxidative enzyme glutathione peroxidase on an average twice, which should be borne in mind in evaluating the efficiency of treatment.
Oxidative modification of low density lipoproteins and tissue lipids has been proposed to be involved in the pathogenesis of atherosclerosis. We examined human atherosclerotic lesions of various stages from fifteen victims of acute heart failure and detected substantial amounts of oxygenated fatty acids in the tissue ester lipids. The degree of lipid oxygenation correlated with the stage of advancement of the lesion. More than 85% of the oxygenated fatty acids were localized in the cholesterol esters, whereas phospholipids contained only small amounts. Structure elucidation of the oxygenation products indicated a nonspecific product pattern of various isomers of keto- and hydroxy-octadecadienoic acid. The data presented suggest an involvement of lipid peroxidation in the pathogenesis of atherosclerosis and indicate that the majority of the oxygenation products are formed via nonspecific, non-enzymatic reactions possibly initiated by the action of a 15-lipoxygenase.
The paper provides the results of 3-month probucol (lipomal) treatment of patients with coronary heart disease concurrent with Types 2a and 2b hyperlipidemia. There were 20% and 17% decreases in total cholesterol and low density lipoprotein cholesterol levels, respectively. The drug failed to affect the levels of high density lipoprotein cholesterol and triglycerides. Having antioxidative properties, probucol significantly enhances the activity of the antioxidative enzymes superoxide dismutase and glutathione peroxidase, which controls the efficacy of coronary heart disease patients with hyperlipidemia.
Primary (dienic conjugates) and secondary (malonic dialdehyde) products of plasma lipid peroxidation were measured and the activity of antioxidative enzymes (glutathione peroxidase and superoxide dismutase) in erythrocytes was determined in 96 patients with chronic heart failure due to ischemic heart disease and rheumatic heart disease. Heart failure was found to show elevated plasma lipid peroxidation product levels, mostly in Stages I and IIA. Whereas in Stage IIB, the product levels became lower and in Stage III, they reached the control values. Similarly, the activity of superoxide dismutase varied with the stages of heart failure. That of glutathione peroxidase increased with circulatory decompensation development, reaching the maximal level in Stage IIB, then decreased down to the values observed in the control groups of patients without heart failure. The changes detected were not related to the causes of heart failure.
Lipoproteins (very low, low and high density) purified from canine fresh plasma produced relaxation of isolated dog coronary artery and rabbit aortic ring segments precontracted with potassium, 30 mM or phenylephrine, 10(-6) M, respectively. No apparent species-specific effects of lipoproteins were revealed and they produced relaxation of other species vessels as well, which differed quantitatively. No apparent endothelium-dependent relaxation produced by animals' lipoproteins was evident. The interference of lipoproteins with some steps in electromechanical coupling is suggested which seemingly result to decrease in excitability of voltage and receptor operated calcium channels of smooth muscle cell membrane. The role of lipoproteins seems to be in maintenance of low level of smooth muscle cell membrane excitability.
Feeding of rabbits with a cholesterol preparation containing 3-5% of cholesterol autooxidation products promotes elevation of plasma cholesterol and atherogenic low- and very-low-density lipoproteins as well as accumulation of neutral lipids (largely, of cholesterol ether) in hepatocytes and intramural arteries of the myocardium. The development of massive aortic lipoidosis can be also attributed to the intake of relevant products. The similar dose of non-oxidized cholesterol did not induce marked or any changes at all in rabbits lipid metabolism and aortic status. The evidence obtained indicates an essential role of food exogenic products of cholesterol oxidation in mechanisms of hypercholesterolemia development and atherosclerotic involvement of vascular walls.
Lipid accumulation in the rabbit liver and myocardium has been investigated by histochemical and biochemical methods. The rabbits received cholesterol that contained 5% of autooxidation products or purified cholesterol. Lipid accumulation took place in the liver and intramural myocardial vessels during feeding of rabbits with autooxidated cholesterol. Feeding with pure cholesterol free from autooxidation products caused but slight changes or no changes at all.