Publications by authors named "Kalishevskaia T"

The effect of modified forms of vasopressin (MFV) that do not possess hormonal activity on homeostasis in rats was studied. One of the major effects of vasopressin (AVP) and its analogs on the blood clotting system, changes in fibrinolytic activity (FA) and the activity of plasminogen activator (APA), depends on modifications of the amino acid sequence in the peptide molecule. The presence of glycinamide in the AVP molecule enhances FA and APA.

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Using two models of experimental thrombosis (arterio-venous shunt and Wessler's model) the effect of plasmin and its combination with alpha-adrenoreceptor antagonists on the formation of thrombus was studied on white rats. It was established that the efficacy of prophylactic of thrombosis by plasmin only was low: middle ball of thrombosis was 2.5-3.

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Effects of vasopressin, its C-terminal fragments and derivatives on the system of hemostasis were studied in rats. Modification of amino acid sequence in vasopressin molecule led to distinct alterations in main peptide properties. Presence of ring structure in the peptide molecule appears to be obligatory to increase the content of factor VIII in blood, while absence of glycine in side chain caused a decrease in the rate of fibrinolysis and in activity of plasminogen activators.

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A change in the response of the blood coagulation system to the intravenous injection of vasopressin (AVP), DDAVP and DGAVP has been studied in the experiments on white rats. Intensification of the procoagulant activity on AVP is of the dose-dependent character. Maximal effect is observed 5-15 min after i.

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Affinity chromatography on heparin-Sepharose was used to isolate two forms of antithrombin III(AT) from human, bovine, rabbit and rat blood plasma. The two isolated forms of AT are the major form. AT alpha, making up to 90% of the whole inhibitor molecule, and the minor form, AT beta (10% of AT).

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Participation of central and peripheral++ cholinoreceptors in responses of blood coagulation system to intravenous vasopressin injection has been studied in experiments on white rats. Vasopressin was injected in combination with atropine and metacine Intensification of the procoagulant activity, that was observed 15 min after vasopressin injection (4 micrograms/kg), was practically retained during cholinergic blockade. The intensification of fibrinolytic activities as a result of an increase in the level of plasminogen activators in blood, is to a great extent blocked by atropine rather than by metacine.

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The participation of plasmin active site in the trigger's mechanisms of the compensatory reaction of haemostasis system on this enzyme was studied in the experiments on white rats and rabbits using intravenous injection and perfusion of the humorally isolated carotid sinus are with intact innervation. Native enzyme, the enzyme with reversibly (acylated plasmin) and irreversibly (diisopropylphosphoryl plasmin) blocked active site were used. It was ascertained that the development of the compensatory reaction of haemostasis system on plasmin, manifested by hypercoagulation and depression of fibrinolysis, is conditioned by the proteolytic activation of the vascular wall receptors.

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Low molecular weight heparin (Mr 8 kDa) was prepared from conventional heparin (Mr 18 kDa) by the chromatography on DEAE-sephadex with the recovery of 56%. Low molecular weight heparin had less affinity to antithrombin III than unfractionated heparin and had less anticoagulant and anti-IIa activities. The anti-Xa activity of low molecular weight heparin exceed by 17% the activity of conventional heparin.

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The electrophoretic and spectral analyses have been used to show the possibility to form a complex consisting of doxorubicin and adriamycin with heparin, the molar ratio being 6:1 and pH 4.8-7.4.

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The influence of antithrombin III on hemostasis and renal function was studied in experiments on rats with nephrotic syndrome. The development of nephrotic syndrome was accompanied by the activation of blood coagulation and appearance of acquired antithrombin III deficiency due to its loss with the urine. The replacement therapy by bovine antithrombin III at a dose of 25 U/kg a day for 10 days decreased the signs of excessive thrombinogenesis in experimental animals and increased the amount of thrombin-antithrombin III complexes in the blood flow.

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Heparin-regulated alpha-thrombin ability to activate the response of the anticoagulation system has been studied by the perfusion of sinocarotid area of rabbits with DIP-alpha-thrombin-heparin complex. In a series of experiments the area was perfused with 1.8 micron DIP-alpha-thrombin and significant changes in anticoagulation parameters have been registered in systemic circulation.

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Electrical stimulation of the hypothalamic dorsomedial and wentromedial nuclei induced an activation of the coagulating system in rats. Plasmin in the vascular bed increased the electrical activity of medial and mamillary hypothalamic neurons, the activity coinciding in time with the maximal level of the blood hypercoagulating response. The activation does nor occur after plasminogen administration.

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It is shown that the damage of sarcoma 45 cells at different stages of cell life cycle occurs under the effect of vinblastine treatment against a background of higher activity of the blood anticoagulating system. A decrease in the mitotic activity, mitosis accumulation in prophase and especially in the metaphase as well as essential changes in the interphase cell ultrastructure are detected.

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The influence of plasmin on blood coagulation in fishes has been studied. The plasmin administration in dose 250 conditional units has been shown to evoke hypercoagulation already on the 5th minute after injection. This defence reaction on the plasmin excess in blood flow was excluded by the preliminary administration of alpha- as well as beta-adrenoblocators.

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The strong depressive effect of vinblastine on the rat sarcoma 45 growth and intensification of this effect by the combination of vinblastine treatment with the activation of the blood anticoagulating system (BAS) were found. Vinblastine had no negative effect on the BAS activation process and induced no persistent changes in the qualitative content of leucocytes in the peripheral blood.

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