[Acceptance of cholesterol by high density lipoproteins in people with dys-alpha-lipoproteinemia and the possible role of apoprotein E in this process]. / Aktseptsiia kholesterina lipoproteinami vysokoi plotnosti u lits s dis-alpha-lipoproteinemiei i vozmozhnaia rol' v étom protesse apoproteina E.

Both subfraction "2" of high density lipoproteins (HDL2) from patients with hypo-alpha-lipoproteinemia and subfraction HDL3 from persons with normal content of cholesterol were shown to accept the erythrocyte membranes cholesterol in vitro. Under these conditions HDL3 subfraction was transformed into HDL2-like particles, where content of unesterified cholesterol and its esters was increased simultaneously with enlargement of the particles size. The HDL subfraction, isolated from persons with high content of cholesterol, did not accept cholesterol under the experimental conditions. Apoprotein E, containing in the HDL subfractions, was not responsible for the particles cholesterol-accepting properties. Apoprotein E itself was capable of cholesterol elimination from erythrocytes as well as of cholesterol esters from HDL3 and HDL2-like particles with formation of a specific complex.

[Participation of apolipoprotein E in the transport of cholesterol esters]. / Uchastie apolipoproteina E v transporte éfirov kholesterina.

It is established in the in vitro experiments that subfraction of HDL3 is able of accepting cholesterol from the atherosclerosis-afflicted aorta intima. Apoprotein E has no effect on the acceptance of cholesterol from the intima by HDL3 particles. The role of the protein under its joint incubation with the aorta intima and HDL3 is reduced to the uptake of cholesterol esters from HDL3-particles enriched by cholesterol. It is assumed that apoprotein E under certain metabolic conditions can transfer esterified cholesterol from HDL-particles on other lipoproteins as well as into tissues impoverished in the cholesterol content.

[Impairment of cholesterol-acceptor function of high density lipoproteins in patients with ischemic heart disease]. / Narushenie kholesterin-aktseptornoi funktsii lipoproteidov vysokoi plotnosti u patsientov s ishemicheskoi bolezn'iu serdtsa.

An ability of high density lipoproteins HDL3 to accept cholesterol from erythrocyte membranes was studied in healthy persons and in patients with ischemic disease of heart. The cholesterol-acceptory function was estimated as follows: by incorporation of fluorescent probes (cholestatriene and pyrene) into particles of HDL3, by elimination of cholesterol from erythrocyte membranes and by increase of the lipoproteins size evaluated using the method of quazi-resilient dispersion of laser light. In ischemic disease of heart the property of high density lipoproteins, specifically of HDL3 fraction, to accept cholesterol from cell membranes was impaired. Middle size of HDL3 particles was decreased in the patients with ischemic heart disease as compared with that of healthy persons.

[Measurement of dimensional distribution of plasma lipoproteins in human blood]. / Izmerenie raspredeleniia po razmeram lipoproteidov plazmy krovi cheloveka.

Possible application of optical mixing method to the investigations of distribution of lipoprotein (LP) particles according to their dimensions is shown. Sensitivity of the method for discovering changes in these distributions at the incubation of lipoprotein particles under different conditions was revealed. It has been shown in particular that when incubating low density lipoproteins (LDL) with erythrocytes the donor properties of LDL in relation to cholesterol, and when incubating high density lipoproteins (HDL) with these cells a more complicated picture is observed. HDL isolated from hypercholesterolemic plasma show the donor properties, and those isolated from the plasma with normal cholesterol level--the acceptor ones. In both cases a high level of aggregatability for total HDL fraction is observed.

[Reactions of high-density lipoproteins and their subfractions with the intimas of atherosclerotic human aortas]. / Vzaimodeistvie lipoproteidov vysokoi plotnosti i ikh podfraktsii s intimoi aorty cheloveka, porazhennoi aterosklerozom.

A ratio of cholesterol esters to free cholesterol was decreased in the total fraction of high density lipoproteins (LPHD) after incubation of the fraction with human aorta intima impaired by atherosclerosis. The same alterations occurred in the reaction of aorta intima with the fraction LPHD3. During incubation of the intima with LPHD2 less distinct decrease was observed in the ratio of cholesterol esters to free cholesterol. The decrease in the ratio of cholesterol fractions, found both in total LPHD and LPHD3, was caused by transfer of free cholesterol from intima cells to LPHD. Thus, LPHD (namely LPHD3 fraction) were able to accept free cholesterol from aorta intima cells; this mechanism is apparently responsible for protective effect of LPHD in atherogenesis.

[Blood plasma lipoextraction as a method of lipid removal from atherosclerotic lesions of the aorta in rabbits]. / Lipoékstraktsiia plazmy krovi kak metod udaleniia lipidov iz ateroskleroticheskikh porazhenii aorty u krolikov.

The effect of repeated lipoextraction of their own blood plasma on regression of the atherosclerotic process was studied in rabbits with experimental hypercholesterolemia 2 months after they had been fed cholesterol. The blood plasma cholesterol level at the end of the experiment was lower in the experimental animals than in the controls, whereas the results of morphological examination of the aortic areas involved in atherosclerosis showed that repeated removal of lipids from the blood plasma promotes rapid regression of experimental atherosclerosis in the experimental animals.

[Lipid extraction from blood plasma and the subsequent administration of the autologous delipidized plasma as a possible agent for treating atherosclerosis (an experimental study)]. / Ekstraktsiia lipidov iz plazmy krovi i posleduiushchee vvedenie v organizm sobstvennoi delipidirovannoi plazmy kak vozmozhnoe sredstyo lecheniia ateroskleroza (éksperimental'noe issledovanie).

A method for the delipidization of blood plasma of rabbits and dogs with diethyl ether with its subsequent reinfusion into the animal's body is described. Triglycerides and cholesterol were mainly extracted from blood plasma, and only 1/3 of phospholipids. In dog experiments the plasma delipidization procedures led to a decrease of the cholesterol content in the overall fraction of atherogenic lipoproteins of low and very low density and an increase of the cholesterol content in antiatherogenic lipoproteins of high density. The lipoextraction procedures are harmless and may be employed for reducing the blood lipid level.

[Nature of the lipoprotein antigen responsible for the development of resistance to experimental atherosclerosis following its use in immunization of newborn rabbits]. / O prirode lipoproteidnogo antigena, otvetstvennogo za razvitie ustoichivosti k éksperimental'nomu aterosklerozu posle immunizatsii im novorozhdennykh krolikov.

In order to develop a tolerance to experimental atherosclerosis newborn rabbits were immunized with various fractions of atherogenic lipoproteins (lipoproteins of low density, lipoproteins of very low density and total fraction of these lipoproteins), isolated from blood serum of adult rabbits with experimental hypercholesterolemia. The tolerance to atherosclerosis proved to be achieved in immunization with lipoproteins of very low density. The lesser effect was observed using the total fraction of lipoproteins. The tolerance was not developed in immunization with lipoproteins of low density.

[Cholesterol metabolism in rabbits with resistance to experimental atherosclerosis acquired by immunological treatment]. / Osobennosti metabolizma kholesterina u krolikov s ustoichivost'iu k éksperimental'nomu aterosklerozu, vyzvannoi immunologicheskim putem.

Development of resistance to experimental atherosclerosis due to immunization of newborn rabbits with homologous fraction of beta- and pre-beta-lipoproteins was accompanied by increased oxidation of cholesterol to biliary acids and by accelerated excretion of cholesterol. The phenomenon appears to be caused by two mechanisms: 1 (cholesterol, occurring in the fraction of free lipoproteins "unblocked" by the antibody (immunzied animals), is more readily oxidized to biliary acids in liver tissue than cholesterol, occurring in the autoimmune complex "lipoprotein-antibody" (non-immunized animals)); 2) the enzymes and biological systems, responsible for elimination of cholesterol from an organism (oxidation to biliary acids, excretion with bile), are activated after immunization of the newborn animals by the lipoprotein fraction endriched with cholesterol.