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Biomedical subjects

V L Leĭtin

Publications and source records attributed to V L Leĭtin.

At least 19 recordsLinked to original sources
PubMed1989

[The role of thrombocyte prostanoids and products secreted by dense granules in the platelet attachment, spreading and aggregation on collagen substrates].

The role of platelet prostanoids and substances released from dense bodies (ADP and serotonin) in the initial attachment, spreading and aggregation of platelets on surfaces coated with I, III, IV and V genetic types of collagen was investigated. A positive linear correlation was found to exist between thrombi-like aggregate formation on collagen substrates and platelet prostanoid synthesis. No correlation was established between platelet aggregate formation and 14C-serotonin release. The cyclooxygenase inhibitor indomethacin and the antagonists of PG endoperoxides and TXA2 (13-APA and BM 13.177) completely block thrombi-like aggregate formation. Neither 13-APA nor BM 13.177 affect platelet spreading, while indomethacin inhibits this process by 25%. The ADP-scavenger CP/CPK inhibits platelet aggregation and spreading by 25-30%. The inhibitors of cyclooxygenase and CP/CPK do not influence the initial attachment of platelets. The data obtained suggest that thrombi-like aggregate formation on collagen substrates is mediated by the synthesis of PG endoperoxides and TXA2; however, in platelet spreading this synthesis plays a limited role. Spreading and aggregation of platelets on collagen substrates is only partly mediated by ADP and serotonin. Initial attachment of platelets does not depend on ADP and serotonin release and PG endoperoxide/TXA2 synthesis.

Adenosine Diphosphate↗
PubMed1989

[Stimulation of spreading and aggregation of platelets on immobilized type V collagen: mechanisms depending on Ca2+ and protein kinase C].

The effects of phorbol ester (PMA) and stable prostaglandin endoperoxide analog (U46619) on platelet interaction with a surface coated with monomeric type V collagen (CV substrate) and free Ca2+ concentration in platelet cytoplasm ([Ca2+]in) have been studied. In the absence of PMA and U46619, the discoid and spherical platelets from suspension are attached to CV substrate but are incapable of spreading and aggregation on the substrate. An addition of PMA (0.15-1.5 nM) or U46619 (1.5 microM) to the reaction mixture stimulates platelet spreading and the formation of multilayer (thrombi-like) aggregates on CV substrate. Using the fluorescent probe Quin 2, it was found that U46619 (0.1 microM) increases [Ca2+]in from the basal level (100-120 mM) to 600 nM. PMA (0.75-15 nM) exerts only a slight effect increasing [Ca2+]in by 30-40 nM. The data obtained suggest that the PMA-induced spreading and aggregation of platelets on CV substrate can occur via activation of protein kinase C at relatively low [Ca2+]in values. These results also testify to the existence of a substrate-independent mechanism of spreading of platelets activated in suspensions by soluble inducers.

Aminoquinolines↗
PubMed1989

[Interaction of thrombocytes with immobilized collagen in the vascular wall (a model for step-by-step study of formation of parietal thrombi)].

Scanning electron microscopy was used to examine the interaction of platelets with types I, III, IV, and V human collagens (CI, CIII, CIV, and CV substrates) immobilized on the surface of cultural plates. Basic differences were found in the activity of collagen substrates against platelets. On the CV substrate, virtually all the adhesive platelets were in a non-spreading++ state, i.e. at the stage of initial attachment to the spread. The CIV substrate showed initial attachment, spreading, and attachment of platelets from the suspension to the spread platelets. In addition to the processes occurring at the CIV substrate, the CI and CIII substrates produced multilayer platelet aggregates on the strata of spreading platelets (thromboid aggregates). The surfaces covered with various types of collagens are an adequate model for quantitative step-by-step study of the formation of parietal thrombocytic thrombi and of mechanisms of this process control.

Blood Vessels↗
PubMed1987

[Mechanisms of inhibition of vascular-platelet hemostasis by salivary gland secretion of the medicinal leech Hirudo medicinalis].

The mechanism of inhibition of the vascular-platelet stage of hemostasis by medicinal leech salivary gland secretion was studied. It was shown that the secretion blocks platelet adhesion on the surface of collagens belonging to different genetic classes, inhibits the primary attachment of platelets and completely suppresses their spreading on collagen surface. Whatever its antithrombin activity, the leech secretion inhibits platelet aggregation stimulated by various inductors, e. g., ADP, prostaglandin endoperoxide analog U-46619, Ca2+ ionophore A23187, arachidonic acid. The secretion possessing the antithrombin activity causes a greater inhibition of the thrombin-stimulated aggregation than that devoid of this activity. Leech secretion stimulates adenylate cyclase of platelet membranes in a receptor-mediated fashion and increases the level of cAMP. The active substance is a low molecular weight, thermostable trypsin-resistant fraction of the secretion. Stimulation of adenylate cyclase is not mediated by adenosine receptors. It is supposed that the mechanism of this activating effect involves platelet prostaglandin receptors.

Adenylyl Cyclases↗
PubMed1984

[Inhibiting action of anti-arrhythmia agents of the phenothiazine series--etmozin and its diethylamino analog--on platelet aggregation and metabolism of endogenous arachidonic acid].

Effect of the cardiotropic drugs of the phenothiazine series ethmozine, and its diethylamine analogue (DAAE), on platelet aggregation and formation of arachidonic acid metabolites has been studied. Both drugs inhibit the ADP-induced aggregation in the platelet-rich plasma. Ethmozine inhibits only the second (irreversible) wave of aggregation, while DAAE inhibits both the first (reversible) and the second one. 50% inhibition (ID50) of the second wave of aggregation is observed at the following concentrations of the two agents: 300-500 micrograms/ml (ethmozine) and 20 micrograms/ml (DAAE). DAAE completely inhibits the irreversible aggregation of platelets washed off plasma, induced by arachidonic acid (ID50 approximately 30 micrograms/ml) and Ca2+-ionophore A23187 (ID approximately 55 micrograms/ml); the aggregation, induced by thrombin is inhibited by 80-90% (ID approximately 130 micrograms/ml). Formation of arachidonic acid metabolites in platelets effected by these inducers was measured by the accumulation of malondialdehyde (MDA). DAAE fails to inhibit MDA formation induced by exogenous arachidonic acid, but completely prevents the synthesis of MDA induced by A23187 and thrombin. These data suggest that DAAE inhibits the release of endogenous arachidonic acid from membrane phospholipids catalysed by phospholipase A2, but does not affect its subsequent metabolic transformations. In all probability, ethmozine and DAAE, just as other phenothiazines, affect platelets via the inhibition of Ca2+-calmodulin-dependent reactions and processes.

Adenosine Diphosphate↗
PubMed1984

[Thrombocyte interaction with a collagen substrate: the role of thrombocyte-synthesized prostaglandin endoperoxides and thromboxane A2].

The effects of (i) the exogenous arachidonic acid (AA), (ii) stable prostaglandin endoperoxide analogue--U46619, and (iii) cyclooxygenase inhibitor--aspirin on the interaction of platelets with a surface coated with fibrillar calf skin collagen were studied using scanning electron microscopy. AA and U46619 stimulate massive spreading of platelets (on the collagen substrate and formation of surface-bound multilayer (thrombi-like) aggregates. The stimulation of spreading and formation of thrombi-like aggregates by AA correlate with the thromboxane A2 (TXA2) synthesis in platelets. Unlike AA, U46619 induces these processes without transformation into TXA2 and stimulation of its synthesis in platelets. Cyclooxygenase inhibitor--aspirin prevents the AA-induced platelet spreading, formation of the surface-bound thrombi-like aggregates, and TXA2 synthesis. In the absence of soluble platelet inducers, aspirin inhibits the substrate-induced spreading, but doesn't affect the initial attachment of nonactivated platelets to the collagen substrate.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1984

[Thrombocyte adhesion and aggregation on surfaces coated with human type-I, -III, -IV and -V collagens].

Human collagens of type I, III, IV, and V (CI, CIII, CIV, and CV) can be localized in different anatomic structures of the vessel wall. To investigate the role of vascular collagenous components in mural thrombus formation, the authors studied platelet adhesion to the wells of Falcon culture plates coated with: a) monomeric CI, CIII, CIV, and CV; b) fibrillar CI and CIII, and c) amorphous CIV and CV. On monomeric and amorphous CV, only initial attachment takes place, i.e. platelets bind to the surface without subsequent spreading. Platelet adhesion on monomeric and amorphous CIV proceeds more actively: the total level of adhesion is substantially higher than on CV, with up to 75% of adherent platelets spread out and single unspread platelets from suspension attached to the upper surface of spread platelets. On monomeric and fibrillar CI/CIII, formation of large multi-layer (thrombi-like) aggregates, with spread platelets at the basis, takes place along with processes characteristic for adhesion on CIV/CV. On the contrary, only fibrillar but not monomeric CI and CIII induce platelet aggregation in suspension. The data suggest that the ability of CI and CIII to induce platelet aggregation is fully conditioned by the genetic type of collagen and requires a simultaneous multivalent platelet-collagen interaction, which can be achieved by surface immobilization of collagen or formation of fibrillar structures in suspension.

Blood Platelets↗
PubMed1984

[Secretion of the salivary glands of the medicinal leech Hirudo medicinalis inhibits ADP-induced aggregation of human platelets and platelet adhesion to a collagen-coated surface].

As was earlier demonstrated, secretion of medical leech exhibits high antithrombin activity of hirudin and inhibits contact activation of factor XII. Attempts were made to investigate the effects of the leech secretion on (i) the ADP-induced aggregation of platelets in suspension, registered by photometry according to Born, and (ii) platelet adhesion to the calf skin collagen-coated surface measured by scanning electron microscopy. The following results were obtained: 1) the secretion at doses of 0.13 vol % and 0.75 vol % inhibits the ADP-induced aggregation of gel-filtered human platelets by 50 and 97%, respectively; 2) the secretion inhibits the total adhesion and initial attachment of the gel-filtered platelets to the collagen substrate by 60-70% (dose 0.1-1.0 vol %) and 87-88% (dose 10 vol %); 3) platelet spreading on the collagen substrate and adhesion of the platelets from suspension to the upper surface of the spread platelets are inhibited by the secretion as well, but these effects are not statistically significant. The data obtained suggest that the secretion contains components which inhibit both the coagulating and platelet-vascular wall pathways of hemostasis.

Adenosine Diphosphate↗
PubMed1982

[Binding of low density lipoproteins (LDL) to platelets].

Binding of LDL to platelets was studied by two independent methods, radioactive and flow cytofluorimetry, using 125I- and fluorescently labelled RITC-LDL. Saturation of 125I- and RITC-LDL binding to platelets, inhibition of binding by unlabelled LDL and a lower inhibitory effect of unlabelled HDL evidence the existence of a limited number of binding sites specific for LDL in platelets. Unlike nuclear cells platelets do not degrade LDL. The binding of LDL to platelets is reversible and independent of Ca2+. The decrease of total binding level at 4 degrees and the absence of heparin effect on the release of bound LDL suggest LDL incorporation into platelets.

Blood Platelets↗
PubMed1981

[Model system for studying thrombocyte interaction with the reconstructed vascular wall].

A new model system is suggested which is a partial reconstruction of normal, locally and vastly injured vessel walls on the basis of fibrillar collagen grown cultures of endothelial cells. The kinetic curve of adhesion on collagen of gel-filtered human platelets reaches saturation within 40 min. During adhesion the shape of collagen bound platelets changes. Acetyl-salicylic acid and platelet free serum inhibit adhesion. Endothelial cells are nonadhesive to platelets; they do not affect the platelet adhesion to the intercellular areas covered with fibrillar collagen.

Animals↗
PubMed1978

[Albumin mRNA from rat liver cells. Analysis of immunoadsorption of individual polyribosomes].

The analysis of albumin polyribosomes immunoadsorption is carried out using "sandwich" immunoadsorbents prepared on the basis of two aminobenzylcelluloses: commercial (paraaminobenzylcellulose) and synthesised (methaaminobenzyloxymethylcellulose). A method is worked out which is good for the estimation of the adaptibility of different aminobenzylcellulose preparations as an insoluble basis for the immunoadsorbent. Major properties of the "sandwich" sorbent (the accessible capacity and specificity) and the percent of isolated individual polyribosomes are found to be interrelated and determined by conditions of the immunoadsorption reaction. The increase of polyribosomes and sorbent concentrations and their ratio in the incubation medium results in the increase of the sorbent accessible capacity and the decrease in the inspecific adsorption but at the same time the percent of adsorbed polyribosomes decrease too. The "excess" of adsorbent with respect to polyribosomes, participating in the binding reaction, is necessary for the quantitative isolation of individual polyribosomes.

Albumins↗