Biomedical subjects
Publications and source records attributed to V N Titov.
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In this article the method of definition of double binders in lipids of blood serum in patients with different diseases basically atherosclerosis and ischemic heart disease, with use titration by ozone is given. The received data testify to an opportunity of use of this method in the diagnostic purposes.
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It is suggested that intracellular deficiency of polyenic fatty acids (FA) is the biochemical basis of atherosclerosis. Its cause in the presence of abundant blood polyenic FA as cholesterol esters (cholesterol-esterified polyenic FA) is blockade of apoB-100-receptor endocytosis. The occurrence of polyenic FA deficiency in phylo- and ontogenesis and the cell adaptation reactions which accomplish the cell transfer and receptor absorption of polyenic FA are considered. The pathogenesis of atherosclerosis is a long-term adaptation to deficient cellular essential FA. At the same time the cells form a plasma membrane, synthesize thromboxanes, prostaglandins, and leukotrienes from omega-9-dihomo-Y-linolenic FA rather than from essential omega-6-arachidonic and omega-3-eicosapentaenic acids. This adaptation process determines all metabolic disturbances which are peculiar to atherosclerosis.
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AIM: To reveal the metabolic parameters of lipoproteins (L), which determine the benefits of hypolipidemic effects of simvastatin (S) and fluvastatin (F); to trace changes in the activity of lecithin-cholesterol acyltransferase (LCA) and cholesterol (C) ester transfer (CET) from high density lipoproteins to very low density lipoproteins (VLDL) and low density lipoproteins (LDL) and the levels of apoE in the blood and in some L classes during therapy with the above drugs. MATERIALS AND METHODS: Thirty six patients took S, 10 mg/day, and 25 received F, 20 mg/day, for 3 months. The levels of lipids were measured by enzyme assays, apoprotein (apo) was determined by immunoturbidimetry and immunodiffusion. RESULTS: The hypocholesterolemic and hypotriglyceridemic effect of S (19.6 and 25.5, respectively) and F (19.0 and 30.5%) were similar. With S, the reduction in the blood levels of C and LDL C positively correlated with the baseline apoE levels. With F, it did with C and LDL C before treatment. Lower blood apoE was found with S and F and lower HDL apoE/(VLDL + LDL) ratio was detected only with F. F treatment significantly lowered the activity of CET and LCA; before and after S treatment, they did not differ significantly. CONCLUSION: Analyzing the relationship between the benefits of the hypolipidemic effect and the baseline parameters of L metabolism indicates that the changes in serum C, LDL C and HDL C are due to the composition of HDL particles and the distribution of apoE among different L classes in the patient to a greater degree.
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AIM: To specify characteristics of lipoproteins (LPs) metabolism in patients with diverse forms of hereditary hyperlipoproteinemia (HLP) and determine biochemical tests for their differential diagnosis. MATERIALS AND METHODS: According to the criteria of polygenic hypercholesterolemia (PHCE), family combined hyperlipidemia (FCHL), family hypertriglyceridemia (FHTG) and family hypercholesterolemia (FHCE), 157 patients were selected aged 7 to 70 years of 192 examinees (76 patients with primary HLP and 116 their close relatives). Lipids were measured by enzyme methods, apoproteins (apo)--by immunoturbidimetry and immune diffusion. RESULTS: Compared to healthy subjects, PHCE patients were characterized by higher apoB level and proportion cholesterol (CS)/apoB in very low and low density lipoproteins (VLDL and LDL). In unchanged level of high density lipoprotein (HDL) CS and proportion HDLP CS/apoA1 there were reduced quantities of free HDLP CS, HDLP2 CS and apoA1. In FHCE and FCHL there were also low levels of HDL CS in elevated ones of apoE in (VLDL + LDL). However, in FCHL, contrary to FHCE, the proportion SC (VLDP + LDL)/apoB was as in control group. FHTG patients differed from healthy subjects by diminished HDL parameters: lower HDL CS due to free CS and its esters, apoA1 and proportion HDL Cs/apoA. There were no differences with controls by content of apoB and proportion CS (VLDL + LDL)/apoB, apoE levels in different class lipoproteins. CONCLUSION: Biochemical parameters are proposed which can differentiate various forms of hereditary hyperlipoproteinemia.