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Biomedical subjects

Kh A Khashimov

Publications and source records attributed to Kh A Khashimov.

16 recordsLinked to original sources
PubMed1988

[An immunoenzyme method of diagnosing familial hypercholesterolemia].

A new modification of enzyme immunoassay: enzyme-linked-immunoreceptor assay (ELIRA)--was used to study the activity of LDL-receptors on cultured fibroblasts from 10 patients with elevated plasma cholesterol levels, IHD, accelerated atherosclerosis and xanthomatosis. Four patients were found to have heterozygous form of familial hypercholesterolemia. We have also shown that the results of ELIRA were quantitatively similar to the data obtained by traditional radioisotopic method. This indicates that simple, rapid, inexpensive ELIRA can be used for diagnosis of FH.

Cell Membrane↗
PubMed1988

[Effect of eicosanoids on the accumulation of cholesterol and the proliferation of subendothelial cells in the human aorta].

The effect of prostacyclin and stable thromboxane analog A2 on endothelial culture of human aorta was studied. It was shown that prostacyclin inhibited accumulation of cholesterol in the cells and their proliferation, while thromboxane exhibited an opposite effect. Calcium antagonists potentiated effects of prostacyclin and inhibited them in respect to thromboxane. Screening of a number of synthetic agents affecting arachidonic acid metabolism was carried out. It was found that lipoxygenase inhibitors suppress cholesterol accumulation and proliferation in cells presumably due to enhancement of prostacyclin synthesis and inhibition of leukotriene formation. The balance between various eicosanoids is supposed to be an important factor of atherogenesis regulation, while antiatherogenic effect of calcium antagonists is somehow associated with the impact of eicosanoids on atherogenesis regulation.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1988

[Effect of lipostabil on cholesterol levels in atherosclerotic plaques of the human aorta and the aggregative capacity of thrombocytes (in vitro study)].

It was found out that lipostabil induced decrease in cholesterol contents in both organ and primary culture of human aorta atherosclerotic plaques. This phenomenon was caused by the effect of lipostabil on cellular output of cholesterol. The study of concentration dependence showed that the cholesterol-decreasing effect of lipostabil was maximal at its concentration in the medium over 250 microliter/ml. At such concentration lipostabil had no significant effect on the blood rheology and inhibited to a great extent platelet aggregation induced by phospholipid platelet activating factor and by some other agents.

Anticholesteremic Agents↗
PubMed1987

[Thrombocyte function during the performance of plasmapheresis and immunosorption in patients with familial hypercholesterolemia].

The impact of plasmapheresis (PA) and immunosorption (IS) of low density lipoproteins (LDLP) on platelets was examined in patients with familial hypercholesterolemia. PA and IS sessions resulted in a decrease of platelet counts, aggregation activity in relation to TXA2 analogue, U46619, and capacity for adhesion and spreading over type-4 collagen-coated surface. All effects were of similar markedness in both procedures, i.e. they were unrelated to PA or IS specificity, but rather were due to platelet interaction with extracorporeal circulation circuit. Platelet changes seen immediately after the procedure were transitory. Platelet counts and capacity for aggregation and adhesion were recovered by the time of the next procedure (1 or 2 weeks later). Long-term (more than 6 months') use of PA or IS did not essentially affect platelet counts, aggregation and adhesion, but rather undermined platelet spreading capacity.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1987

[Effect of components of the extracellular matrix on the accumulation of lipids in human cells].

The effect of extracellular matrix components on cholesterol accumulation in different human cells was studied. Insoluble LDL-Heparin-Fibronectin-Gelatin complexes were incubated with human cells: fibroblasts, monocytes, peritoneal macrophages, cells of the aortic wall--endothelial, subendothelial intimal, medial; and total cholesterol content in these cells was determined. It has been demonstrated that components of extracellular matrix being complexed with LDL enhance total cholesterol accumulation in all cell types studied: the highest amount of cholesterol was accumulated by subendothelial intimal cells and peritoneal macrophages. It is suggested that components of extracellular matrix can play an important role in the development of lipid-laden foam cells that are accumulated in the arterial wall in atherosclerotic lesions.

Endothelium, Vascular↗
PubMed1986

Primary culture of human aortic intima cells as a model for testing antiatherosclerotic drugs. Effects of cyclic AMP, prostaglandins, calcium antagonists, antioxidants, and lipid-lowering agents.

Smooth muscle cells isolated from atherosclerotic lesions of human aorta retain in primary culture their intrinsic in vivo characteristics: namely, enhanced proliferative activity and high lipid levels. We have tested the effect of different compounds on [3H]thymidine uptake and on the levels of phospholipids, triglycerides, cholesterol, and cholesteryl esters in cultured aortic cells. Effects, such as the inhibition of cellular proliferation and/or lowering of the intracellular lipid levels which would be regarded as antiatherosclerotic if exerted in vivo, were observed in vitro by the following compounds: dibutyryl cyclic AMP, cholera toxin, forskolin, methylisobutylxanthine, stable prostacyclin analogues, prostaglandins E2 and D2, verapamil, reserpine, alpha-tocopherol, butylated hydroxytoluene, lipostabil, and high density lipoproteins. In this paper, we discuss the possibility of using a primary culture of smooth muscle cells from an atherosclerotic human aorta for testing drugs for possible antiatherosclerotic activity.

Antioxidants↗
PubMed1986

[Effect of plasmapheresis on plasma hormone levels in patients with hereditary hypercholesterolemia].

It is shown that plasmapheresis in the volume of 30-46 ml/kg using 2997 cellular separator (IBM) does not significantly reduce testosterone, estradiol, aldosterone, parathyroid hormone and calcitonin concentrations. The initially high level of insulin and C-peptide was reduced, angiotensin-I concentration lowered and somatotropic hormone concentration doubled. It is suggested that plasmapheresis stimulates lipolytic and anabolic processes in the organism.

Adult↗
PubMed1986

Intimal cells and atherosclerosis. Relationship between the number of intimal cells and major manifestations of atherosclerosis in the human aorta.

The subendothelial intima of human aorta is populated by cells of various shapes. Round and ovoid cells which are lymphocyte- and monocyte-like hematogenous cells account for less than 5% of the cell population. The bulk of the intimal population (over 95%) is made up of cells that can be described as elongated, stellate, elongated with side processes, and irregularly shaped. To identify these morphologic forms, the authors have used target electron microscopy. It has been established that elongated cells devoid of side processes possess all the ultrastructural features of differentiated smooth muscle cells: a developed contractile apparatus in the form of microfilament bundles with dense bodies occupying most of the cytoplasm, basal membrane surrounding the whole of the cell, and micropinocytotic vesicles along the plasma membrane. The other morphologic forms have an ultra-structure that allows us to identify them as so-called modified smooth muscle cells. They differ from the typical smooth muscle cells in that they have fewer contractile structures and a more developed biosynthetic apparatus. Some of stellate and irregular shaped cells are utterly devoid of contractile structures. To quantitate the number of cells of different morphologic forms, the authors used alcoholic-alkaline dissociation of prefixed intima. It was established that the intimal population is multiplied at the site of an atherosclerotic lesion, the number of stellate cells being increased much more substantially, compared with other morphologic cell forms. It was found that an increase in the number of stellate cells is related to such sequelae of atherosclerosis in aorta as intimal thickening, deposition of lipids, and an increased amount of collagen. There was a high positive correlation between the alteration in the stellate cell number occurring in the intima and the above-mentioned parameters (correlation coefficients were 0.732, 0.800 and 0.953, respectively). The correlations between these indexes and the total number of intimal cells or the number of cells belonging to each of the other morphologic forms were not so high. A multivariate analysis gave similar results. Thus, it may be suggested that stellate cells are the principal cell type involved in the disease. This report discusses the origin of stellate and other intimal cells and their role in atherogenesis.

Adult↗
PubMed1984

[Changes in the physical load tolerance of stenocardia patients taking obzidan, korinfar and izoptin separately and together].

Changes in exercise tolerance under the impact of obsidan, corinfar, isoptin and their combinations were studied in 12 angina patients with the help of bicycle ergometry. The most marked increase in exercise tolerance following the use of a single drug was observed with obsidan (85.1 +/- 35.1%), although corinfar and isoptin also led to a significant elevation in the patients' working capacity (67.4 +/- 14.4% and 49.8 +/- 6.3%, respectively). Combination of isoptin and obsidan brought about no increase in tolerance as compared with obsidan alone whereas the combination of corinfar with obsidan showed the maximal antianginal effect.

Adult↗
PubMed1984

[Functional state of the myocardium during stenocardia induced by isoproterenol].

Hemodynamic changes in healthy subjects versus patients with chronic coronary heart disease are compared. In cases of isoproterenol caused tachycardia, the patients developing angina showed a less prominent beneficial inotropic effect as compared with healthy subjects and angina-free patients. The initiation of drug infusion led to a marked increase in the rheographic index of myocardial contractility; however, already in the initial stages of ST segment depression, this parameter was characterized by a reversed time-course which progressed with the increasing electrocardiographic signs of myocardial ischemia. The degree of the observed impairments of the patients' inotropic response correlated with the severity of myocardial ischemia and the nature of the disease course.

Adult↗