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Biomedical subjects

Z A Gabbasov

Publications and source records attributed to Z A Gabbasov.

At least 19 recordsLinked to original sources
PubMed1998

[Determination of the activity of Willebrand's factor by laser analyzer of platelet aggregation].

A modification of von Willebrand' factor/ristocetin cofactor activity test is proposed. Agglutination of formalin-treated platelets is monitored in the aggregation analyzer from changes in the light transmission in the specimen. The test is sensitive and reproducible. It is intended for clinical laboratories to be used in patients with hematological diseases and the endotheliopathy syndrome of different etiology.

Hemagglutination↗
PubMed1994

[The functional characteristics of the thrombocytes in patients with hypertension and "silent" myocardial ischemia].

Functional platelet characteristics were studied in hypertensive subjects having episodes of silent myocardial ischemia. A total of 36 patients with essential hypertension (EH) stage II (WHO criteria, 1979) underwent echocardiography and 24-h ECG monitoring. Platelet aggregation induced by adenosine diphosphate was assessed by laser aggregation analyzer. It is demonstrated that platelet aggregation in EH patients with silent ischemia was increased 5-fold as compared to healthy subjects and 2-fold versus EH patients without ischemia. No significant differences existed between the two groups by such parameters as systolic or diastolic pressure and left ventricular myocardial mass. An involvement of elevated platelet aggregation can be suggested in the genesis of coronary insufficiency in EH associated with episodes of silent myocardial ischemia.

Analysis of Variance↗
PubMed1992

Three types of naturally occurring modified lipoproteins induce intracellular lipid accumulation due to lipoprotein aggregation.

Low density lipoprotein (LDL) from patients with coronary atherosclerosis and diabetes mellitus as well as in vitro desialylated LDL, glycosylated LDL, and lipoprotein (a) caused a twofold to fourfold rise in cholesteryl ester in cultured human blood monocytes and intimal smooth muscle cells isolated from normal aorta. Native LDL from healthy subjects failed to induce intracellular lipid accumulation. We have demonstrated by laser correlative photometry and gel filtration chromatography that in vivo and in vitro modified lipoproteins form aggregates under cell culture conditions. The degree of modified lipoprotein aggregation directly correlated with the ability of these lipoproteins to elevate the cholesteryl ester content of cultured cells. Modified lipoprotein aggregates isolated by gel filtration induced a threefold to fivefold elevation in cellular cholesteryl ester content. Aggregates of 125I-modified LDL were taken up and degraded fivefold to sevenfold more effectively as compared with nonaggregated lipoproteins. The uptake and degradation of 125I-labeled aggregates were strongly inhibited by unlabeled aggregates, latex beads, and cytochalasin B but not by native or acetylated LDL. These data indicate that uptake of lipoprotein aggregates occurred by phagocytosis. Obtained results suggest that modified lipoprotein aggregation may be the key condition for lipid accumulation.

Cells, Cultured↗
PubMed1992

Three types of naturally occurring modified lipoproteins induce intracellular lipid accumulation in human aortic intimal cells--the role of lipoprotein aggregation.

Blood monocytes or intimal smooth muscle cells from normal aorta were incubated with low density lipoprotein (LDL) from patients with coronary atherosclerosis, or with LDL from diabetic patients, or with lipoprotein(a) (Lp(a)). In each case there was a 2- to 4-fold rise in the intracellular cholesteryl ester content. LDL from healthy subjects failed to induce intracellular lipid accumulation in these cells. LDL from patients with coronary atherosclerosis, LDL from diabetic patients, and Lp(a) form aggregates under cell culture conditions. The ability of these lipoproteins to increase the cholesteryl ester content of cultured cells is directly correlated to the degree of lipoprotein aggregation. When aggregates were removed from the lipoprotein preparations by filtration, the latter became less effective in promoting intracellular lipid accumulation. Incubation of cells with lipoprotein aggregates, isolated by gel filtration, induced a 3- to 5-fold elevation of the cellular cholesteryl ester content. These results suggest that LDL from atherosclerotic patients, or LDL from diabetic patients, or Lp(a) have a tendency to form aggregates and that these aggregates are avidly taken up by intimal smooth muscle cells followed by lipid accumulation. This aggregation tendency may play a role in atherogenesis.

Aorta↗
PubMed1992

Multiple-modified desialylated low density lipoproteins that cause intracellular lipid accumulation. Isolation, fractionation and characterization.

BACKGROUND: The basic differences between sialylated (sialic acid rich) and desialylated (sialic acid poor) human low density lipoproteins (LDL) are not fully defined. It is not known whether there are any differences in the LDL composition of coronary atherosclerosis patients and healthy individuals. EXPERIMENTAL DESIGN: Sialylated (45 to 94% of total LDL) and desialylated (6 to 55%) LDL were separated by affinity chromatography on Ricinus communis agglutinin-agarose, and their chemical composition and physical properties were examined. RESULTS: Sialic acid contents in sialylated LDL fractions of healthy subjects and patients were the same and 1.5 to 3-fold higher than in desialylated LDL. Desialylated LDL had smaller sizes and greater electrophoretic mobility than sialylated ones. Desialylated, but not sialylated LDL, induced 1.5- to 4-fold accumulation of neutral lipids in human aortic smooth muscle cells and human blood monocytes. Subfractions of desialylated LDL containing lower amount of sialic acid revealed higher ability to accumulate lipids in cultured cells. Desialylated LDL contained lower amounts of cholesteryl esters, free cholesterol and triglycerides as compared with sialylated LDL. On the other hand, concentration of di-, monoglycerides and free fatty acids in desialylated LDL was 2 to 3-fold higher than in sialylated lipoproteins. Desialylated LDL fraction was characterized by lower levels of phosphatidylcholine, sphingomyelin, phosphatidylethanolamine, but higher content of lysophosphatidylcholine. Freshly isolated sialylated and desialylated LDL contained equal amounts of thiobarbituric acid reactive substances, but oxidation of desialylated LDL was more pronounced in presence of Cu(2+)-ions. Desialylated LDL had higher level of oxysterols and lower amounts of vitamin A and E. Content of free amino groups of lysine in desialylated LDL of patients was 2-fold lower than in sialylated LDL. This difference was partially due to masking of amino groups caused by conformational change in the tertiary structure of apolipoprotein, partially to chemical modification of amino groups. When subfractionated by density gradient ultracentrifugation, desialylated LDL was represented by higher density particles than sialylated LDL. Sialic acid content in desialylated LDL subfractions decreased with rise of lipoprotein density. Higher density desialylated LDL and in less extent sialylated LDL contained smaller amounts of free and esterified cholesterol and phospholipids. Only the densest subfractions of desialylated LDL from healthy subjects caused intracellular lipid accumulation. Ability of patients' desialylated LDL to accumulate cholesterol in cells increased with particle density. CONCLUSIONS: Extensive biochemical and biophysical analysis performed in this study shows that desialylated LDL differ from these sialylated LDL in many respects. The LDL of coronary atherosclerosis patients differ from those in healthy individuals in several parameters.

Adult↗
PubMed1991

[ADP-induced thrombocyte aggregation in hypertension patients with different degrees of left ventricular hypertrophy].

Adenosine diphosphate (ADP)-induced platelet aggregation was studied in 59 patients suffering from essential hypertension, stages I and II (WHO, 1979) with different degree of left ventricular hypertrophy (LVH) by a new optical method. Using a laser aggregation analyzer the mean aggregate radius was measured in relative units. The left ventricular myocardial mass was estimated by echocardiography. Using laser aggregatograms the significant differences in aggregation responses were revealed with 0.5 microM ADP. In a group of patients without LVH, the aggregation response to 0.5 microM ADP did not differ from that in a group of healthy volunteers. With the growth of LVH from moderate to severe the response increased in succession. The same differences which were not, however, significant were observed with higher ADP concentrations. It was also found that the new method of laser aggregometry is more sensitive than the classic Born method.

Adenosine Diphosphate↗
PubMed1990

[Aggregates of modified low density lipoproteins indicate accumulation of lipids in human aortic intima cells in vitro].

Spontaneous aggregation of glycosylated, desialated, oxidized and malondialdehyde modified low density lipoprotein (LDL) as well as LDL of coronary heart disease patients has been discovered using methods for determination of light transmission fluctuations in suspensions and gel filtration. At the same time; LDL of healthy donors failed to aggregate under conditions of cellular culture. On the other hand, human aortic cells from unaffected intima incubated with modified LDL, but not native LDL of healthy donors, showed a rise in esterified cholesterol levels. There was a strong correlation between the degree of LDL aggregation and intracellular cholesterol ester accumulation (r-0.86, p 0.001, n-21). Removal of aggregates by passing preparations through and 0.1 um filter significantly inhibited the accumulation of cholesterol esters. The obtained data point to the essential, if not decisive, role of LDL aggregation in the processes of lipid accumulation by intimal cells in vitro.

Aorta↗
PubMed1989

Lipoprotein aggregation as an essential condition of intracellular lipid accumulation caused by modified low density lipoproteins.

We have tested a hypothesis that aggregates of modified low density lipoproteins (LDL) play the key role in the accumulation of lipids by cells of unaffected aortic intima. It was demonstrated using analysis of relative dispersion of light transmission fluctuations as well as gel filtration on Sepharose CL-2B that LDL modified by oxidation, glycosylation, desialylation and malondialdehyde treatment form aggregates under the conditions of culture. Native LDL failed to aggregate under the same conditions. It was demonstrated that modified LDL, unlike native LDL, bring about a 2- to 3-fold rise in cholesteryl ester levels of cultured cells. Moreover, direct and strong correlation (r = 0.86) was observed between the degree of lipoprotein aggregation and the amount of cholesteryl esters accumulated. Removal of modified LDL aggregates by filtration through a 0.1 micron filter or gel filtration completely prevented the intracellular accumulation of cholesteryl esters. These findings indicate that LDL aggregates play an essential, if not the decisive, role in the intracellular accumulation of lipids in vitro.

Aorta↗
PubMed1989

Platelet aggregation: the use of optical density fluctuations to study microaggregate formation in platelet suspension.

A new approach to the investigation of microaggregate formation kinetics in platelet suspension is described. The method is based on the analysis of light transmission fluctuations produced by the changes in the number of platelets in optical channel. The relative dispersion of such fluctuations (D) was used as a parameter to estimate the degree of platelet aggregation and to analyze the aggregation kinetics. It was found that a continuous recording of this parameter allows to detect microaggregate formation during spontaneous aggregation and aggregation induced by very low concentrations of ADP (0.05-0.15 uM) in platelet-rich citrate plasma. When 3-10 uM ADP was added to acid citrate-dextrose anticoagulated plasma at pH 6.5, microaggregate formation was detected by increase in D, whereas light transmission decreased by 15-20%. Analysis by scanning electron microscopy and the use of standard inhibitors of aggregation confirmed that in all these cases the microaggregate formation did take place.

Adenosine Diphosphate↗
PubMed1989

[A new highly sensitive method of analysis of thrombocyte aggregation].

The new method for studies of the platelet aggregation kinetics is based on the creation of a platelet stream through the optic canal and on an analysis of fluctuations in the intensity of the luminous flux that has passed through the sample. The relative dispersion of fluctuations in the intensity of the light passed through the sample is suggested as a parameter for the estimation of the platelet aggregation and for analysis of their aggregation kinetics. The method permits recording the platelet aggregation in citrate plasma, enriched for platelets, after exposure to the inductor in very low concentrations (0.05-0.15 microM ADP). Scanning electron microscopy has shown that aggregates are indeed formed in such cases, and they can be recorded from the increase of the relative dispersion in the fluctuations in the passed light intensity but cannot be recorded by Born's optic method.

Adenosine Diphosphate↗
PubMed1989

[Functional state of blood platelets in arterial hypertension and the changes in serotonin-containing cellular granules].

The study was undertaken to examine the status of the granular apparatus and platelet aggregability in 9 healthy donors and 18 patients with arterial hypertension (AH), including 14 with essential hypertension (EH) and 4 with symptomatic forms of AH. Among the patients, a group of 8 EH patients was singled out, who had, compared with normal, reduced relative volumes of electron dense platelet granules (from 17.9 +/- 2.0 to 5.3 +/- 0.6%). The group also showed lower platelet serotonin levels (from 67.3 +/- 5.3 to 17.6 +/- 3.7 ng per 10(8) cells; p less than 0.001) and a 2-fold decrease in the transport factor of acridine orange across the cytoplasmic and granular membranes as compared to normal. A positive correlation was established between the amounts of cellular serotonin and the relative volume of platelet granules (r = 0.850; p less than 0.001).

Adult↗
PubMed1989

[New approaches to the study of thrombocyte aggregation in patients with dilated cardiomyopathy].

A degree of platelet aggregation in patients with dilatation cardiomyopathy (DCMP) with different stages of heart failure (HF) was evaluated with the help of a highly sensitive aggregometer developed in the All-Union Cardiological Research Center AMS USSR. The main advantage of this modification was a possibility to study platelet aggregation in response to small doses of an inductor (e.g. less than 0.2 microM of ADP) that could not be done using routine methods. A significant rise of a degree of platelet aggregation was revealed in patients with 0-I,IIA stages of DCMP and IIB-III stages of HF in response to 0.1 microM of ADP. Platelet aggregation was enhanced with an increase in a HF stage. The addition of a higher concentration of ADP (0.2-0.5 microM) and the platelet aggregation factor (5 and 25 nM) revealed no rise of platelet aggregation in patients with 0-I stages of DCMP and IIA stage of HF. Only in patients with stages IIB-III of HF was a platelet aggregation index significantly raised in response to 0.2 and 0.5 microM of ADP but to a much lesser degree than in the addition of 0.1 microM of ADP.

Adenosine Diphosphate↗
PubMed1988

Evaluation of the ability of intact platelets to accumulate acridine orange.

A new approach to the evaluation of the uptake of fluorescent probes by intact cells is described. Acridine orange (AO) was used because it can be selectively accumulated by serotonin-containing granules of platelets. Analysis of the fluorescence signal allows the estimation of the relative volume of the granules and the equilibrium coefficients for AO transport across the cytoplasm and granule membranes. The following results were obtained for human and rabbit platelets: the relative volumes of the granules were 14 +/- 1% and 29 +/- 2%, the ratios of intragranular-extracellular probe concentration were 2260 +/- 382 and 30,000 +/- 5550, and the cytoplasm-extracellular medium concentration ratios were 375 +/- 60 and 225 +/- 60, respectively.

Acridine Orange↗