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Biomedical subjects

T M Kalishevskaia

Publications and source records attributed to T M Kalishevskaia.

At least 19 recordsLinked to original sources
PubMed1989

[The role of the active center of the enzyme in the triggering mechanism of the compensatory reaction to plasmin].

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.

Acylation↗
PubMed1989

[Heterogeneity of mammalian antithrombin III].

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). The molecular mass of AT beta in all mammalian species under study is by 3-5 kDa lower than that of AT alpha. The isoelectric point for bovine AT alpha lies within the range of 4.95-4.5, whereas that for AT beta--at 5.28-4.76. No significant differences in the progressive antithrombin activity of the major and minor forms of the bovine inhibitor were observed. In contrast, the heparin-cofactor activity of the AT beta-heparin complex exceeds that of the AT alpha-heparin complex--3-fold. The functional differences in the AT forms are due to the differences in their affinities for heparin. It was shown that AT beta exhibits a higher affinity for free and bound heparin.

Animals↗
PubMed1988

[Anticoagulant and antithrombotic effects of low molecular weight heparin].

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. In the experiments on rats it was determined that the biological half-life of low molecular weight heparin exceed two-fold that of the unfractionated heparin. In the modified model of the arteriovenous shunt thrombosis in normal and nephrotic syndrome rats it was shown that the low molecular weight heparin was the most efficient antithrombotic remedy in normal and decreased level of antithrombin III in the organism.

Animals↗
PubMed1988

[Action of doxorubicin and a doxorubicin-heparin complex on the growth and metastasis of experimental tumors and the hemostatic system indices].

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. Doxorubicin and adriamycin had procoagulant properties but the doxorubicin-heparin complex showed an anticoagulant activity. In experiments on rats with the Pliss lymphosarcoma and sarcoma 45 the doxorubicin-heparin complex depressed more efficiently the tumour growth and metastasis spreading. The combination of doxorubicin and the doxorubicin heparin complex with the trypsin-heparin complex which imitate the hyperfunction of anticoagulative system markedly increased the antitumour effects.

Animals↗
PubMed1987

[Replacement therapy of acquired antithrombin III deficiency in experimental nephrotic syndrome].

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. The activation of coagulation in rats with nephrotic syndrome predominantly induced the disturbances of the excretory renal function which could be efficiently corrected by antithrombin III.

Animals↗
PubMed1986

[Effect of heparin on the activation of the anticoagulation system by alpha-thrombin].

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. During perfusion of sinocarotid area by DIP-alpha-thrombin-heparin complex (2 microns) no activation of anticoagulation system was noted. DIP-alpha-thrombin-heparin perfusates contained no endogenic heparin, unlike DIP-alpha-thrombin perfusates. This confirms the absence of anticoagulation system response to DIP-alpha-thrombin. Control perfusion by heparin alone in equimolar concentrations revealed no changes in anticoagulation system. It is assumed that heparin, blocking cation subcentre of the recognition centre for high molecular compounds in the enzyme molecule, prevents the response of anticoagulation system, disturbing the enzyme ability to bind to specific receptors of the vascular walls.

Animals↗
PubMed1985

[Effect of the enzyme plasmin on blood coagulation in fish].

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. Subtle differentiation of adrenoreceptors is supposed to be absent in fishes, nevertheless they play a definite role in regulation of hemostasis system.

Adrenergic alpha-Antagonists↗
PubMed1985

[Role of hypothalamic adrenoreactive structures in regulating the protective reaction to plasmin].

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. The activation of the blood coagulating system is due to an excessive amount of plasmin in the blood and can be suppressed with sympatholytic agents. The plasmin-induced electrical activity is suppressed with aminasin whereas phentolamine administration does not affect the activity though no activation of coagulating system occurs. Absence of humoral hypercoagulating shift in the blood confirms participation of alpha-adrenoreception in peripheral efferents. The increased efferent sympathetic activity seems to be the cause of plasmin-induced hypercoagulation.

Animals↗
PubMed1985

[Light optical and electron microscopic studies of the tumor cells in rats exposed to vinblastine against a background of increased activity of the anticoagulating system].

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.

Animals↗
PubMed1984

[Effect of vinblastine during high activity of the anticoagulating system on the growth of sarcoma 45 in rats and several blood indicators in animals with tumors].

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.

Animals↗
PubMed1983

[Effect of plasmin on the efferent sympathetic activity in rats and rabbits].

The change of efferent sympathetic activity at intravenous administration of plasmin and perfusion of the isolated carotid sinus hes been studied in experiments on rabbits and rats. The correlation between changes of biochemical blood parameters and changes of its activity has been noted. The maximum hypercoagulative effect conforms to maximum increase of sympathetic activity as at intravenous administration so at perfusion. An increase of the efferent sympathetic activity is much higher in case of intravenous plasmin administration than in perfusion of the isolated carotid sinus.

Animals↗
PubMed1981

[Role of medullary nuclei and the vagus nerve in hypothalamic regulation of the anticoagulant system].

Electric stimulation of the anterior and rostral parts of the lateral hypothalamus induced activation of the medulla oblongata n. ambiguus and did not change the activity of the vagus n. gigantocellularis and n. dorsalis. Thrombin administration induced maximal activity in the nn. vagi within 3--5 min and the maximal hypocoagulation during the same time in the blood. A scheme of efferent pathways for the hypothalamic regulation of the anticoagulating system, is suggested.

Animals↗
PubMed1979

[Nature of vagotomy and atropine hypercoagulation].

Bilateral vagotomy and i. v. administration of atropin entailed shortening of total and thrombin time and lowering of fybrinolysis. The vagotomy brought about the changes within 3--15 min, whereas the atropinization evoked them in about 30--60 min. The maximum shortening of total and thrombin time and lowering of fibrinolysis occurred at the moment of highest activity of the cervical sympathetic system. Thereupon these effects in the blood coagulating system seem to be called forth by activity of the sympathetic system after vagotomy.

Animals↗
PubMed1979

[Role of adreno- and cholinoreactive structures of the hypothalamus in regulating blood coagulation and maintaining it in a fluid state].

Electrical stimulation of anterior and lateral hypothalamus as well as acetylcholin injection into the same areas activated the anticoagulating blood system whereas adrenaline injections activated the coagulating system. The electrical stimulation with certain parameters seems to involve cholinoreactive structures of the hypothalamus, shifting the blood potential towards hypocoagulation. The sitmulation of the paraventricular and ventromedial hypothalamic nuclei with the same current activated the blood coagulating system whereas stimulation of the preoptic lateral or medial areas, medial supraoptic nucleus of the hypothalamus induced no changes in the homeostatic system. The data obtained suggest that the regulation of the blood anticoagulating system involves the anterior hypothalamic area, the suprachiazmatic nucleus, and the rostral part of the lateral hypothalamic area.

Acetylcholine↗