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Biomedical subjects

E M Tararak

Publications and source records attributed to E M Tararak.

At least 55 records · Page 3Linked to original sources
PubMed1983

[Dynamics of the activity of energy metabolism and lysosomal enzymes in experimental atherosclerosis (a quantitative histochemical study)].

A quantitative biochemical study of patterns of energy and lysosomic enzymes in cellular elements of the rabbit aorta under induced atherosclerosis showed these enzymes to be activated during earlier atherogenetic stages associated with the formation of atherosclerotic patches in the intima, an evidence of functional adaptation of the aortal wall building up the defence mechanisms against adversary effects of cholesterol and other lipids. Once marked atherosclerotic patches have been formed in the aorta, adaptive potentials of enzyme systems are exhausted and further changes in their activity can result in processes conducive to the development of experimental atherosclerosis.

Animals↗
PubMed1980

[Dynamics of the proliferative activity of aortic cells in the process of the formation of an atherosclerotic plaque].

It was demonstrated by 3H-thymidine histoautoradiography that after 3 weeks of a cholesterol diet the number of labelled endothelial and subendothelial cells in the aorta of rabbits increases sharply. With the gradual development of experimental atherosclerosis (after 6 weeks of the experiment) two types of atherosclerotic patches are found in the aorta, which differe one from the other in the degree of "maturation" and the character of distribution of the proliferating cells. Experiments with "setting apart" of the 3H-thymidine label show clearly the possibility of transformation of the subendothelial cells into lipid macrophages. The main growth of the cell mass of the atherosclerotic patch, however, occurs because the lipid macrophages themselves proliferate. The hypothesis claiming that the subendothelial cells are the precursors of all cell elements forming the patch is discussed.

Animals↗
PubMed1979

[Role of glycosaminoglycans in altering vascular wall permeability for atherogenic lipoproteins].

The relationship between the pattern of distribution of lipoproteins and morphological features of atherosclerotic lesions was demonstrated by histoautoradiographic and histochemical methods in experiments using perfusion in vitro of aortas from atherosclerotic rabbits with atherogenic lipoproteins (LP) labeled in various positions. Accumulation of glycosaminoglycanes (GAG) in the time course of the atherosclerotic process was shown to be the factor contributing to the retention of LP in the vessel wall. At the same time, no GAG accumulation was found in sites of the greatest permeability. Irrespective of the stage of the process, formation of foci of increased permeability was, as a rule, associated with accumulation of poorly differentiated cells. The evidence of primary increase of permeability of the endothelial barrier in the form of activation of the proliferative processes and GAG accumulation was obtained.

Animals↗
PubMed1976

[Effect of ethirazol and parmidine ofn the development of experimental atherosclerosis in rabbits].

Experiments on rabbits which received cholesterol in food for 3-4 months showed an inhibitory effect of ethirazol (bis-methylamide-1-ethyl-pyrazol-3,4-bicarbonic acid) and parmidine (piridinolcarbamate, 2,6-bis-hydroxymethylpiridine bis-n-methylcarbamate) on the development of experimental atherosclerosis: there proved to be a reduction of accumulation of total cholesterol in the aorta and of its atherosclerotic affection. At the same time the blood serum cholesterol, triglycerids and phospholipid content was not significantly changed by these drugs.

Animals↗
PubMed1975

[Histoautoradiographic and biochemical study of the transport of atherogenic lipoproteins in the vascular wall].

Transport of serous pre-beta and beta-lipopropeins (beta-LP) labeled by C14 protein and by C14 lipid into the wall of the aorta was studied histoautoradiographically and biochemically. The aortas of healthy rabbits and rabbits wuth experimental atherosclerosis were perfused in vitro with a medium containing rabbit pre-beta and beta-LP during 6 hours. After perfusion the mark was identified histoautoradiographically in all layers of the aorta. The presence of gradient in distribution of the mark from the inner layers of the aortas towards the outward part of the media indicated that the process of infiltration of the wall of the LP vessel was caused by their penetration from the lumen of the aorta. Nonuniformity in distribution of LP penetrated into the atherosclerotic aorta was noted, which was considered in connection with the changes occurred in the connective tissue of the wall of the aorta in the process of atherogenesis. Results of both morphological and biochemical investigations confirm an increased permeability of the aorta wall for LP in atherosclerosis and also substantiate the assumption about penetration of pre-beta and beta-LP into the wall of the vessel as a whole particle.

Animals↗
PubMed1975

[The histoenzymology of arterial walls under normal conditions and during the development of atherosclerosis].

Investigation of enzymes of the vascular wall in atherosclerosis in man and in experiment should include biochemical studies in combination with histochemical control. It is most probable that the total activity of enzymes in the vascular wall in atherosclerosis depends upon the functional state of smooth-muscle cells. The character of changes in the activity of enzymes in the arteries susceptible to atherosclerosis makes it possible to prognose disturbances in metabolism of the vascular wall and partially to explain the sequency of the development of the atherosclerotic process.

Adenosine Triphosphatases↗
PubMed1975

Historadioautographic and biochemical studies on the transport of atherogenic lipoproteins into the rabbit aortic wall.

Historadioautographic and biochemical studies were undertaken on the transport of 14C-labelled serum very low density and low density lipoproteins (VLDL and LDL respectively) into the aortic wall. Aortas from normal and atherosclerotic rabbits were perfused in vitro with a medium containing VLDL and LDL for 6 hours. Historadioautography revealed the label in all the layers of the perfused aorta. The gradient in the distribution of this label from the inner layers of the aortic wall dawn to the outer part of the media demonstrated that lipoprotein infiltration of the vessel wall is due to uptake of lipoproteins from the aortic lumen. The non-uniform pattern of the distribution of lipoproteins taken up by the atherosclerotic aorta was considered as a result of atherogenesis induced changes in the aortic connective tissue. Both morphological and biochemical studies revealed the increased permeability of the atherosclerotic aortic wall to VLDL and LDL, which appeared to penetrate the walls of blood vessels in the form of intact particles.

Animals↗
PubMedDate not supplied

[Phenotypes of smooth muscle cells in carotid arteries in Takayasu's disease].

The phenotype of smooth-muscle cells (SMC) of carotid arteries in health and Takayasu's disease were studied using immunofluorescence. In contrast to unaffected carotid artery, medial SMC were represented by heterogenic cell population. Many SMC in this disease expressed fibronectin with ED-A sequence, contained cytokeratin 8 and were deprived of h-caldesmon. Similar phenotypic characteristics are typical for SMC of embryonal phenotype. SMC with this phenotype are observed in the thickened intima of the carotid arteries in Takayasu's disease. It is supposed that SMC precursors in arterial media are activated in this disease, migrate into subendothelial layer and are responsible for the thickening of the intima.

Adult↗