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Biomedical subjects

G V Bashkov

Publications and source records attributed to G V Bashkov.

32 records · Page 2Linked to original sources

[The thrombolytic activity of acylated activator complexes of plasmin-streptokinase with different rates of reactivation].

In the experiments on guinea-pigs with venous thrombosis there were studied the fibrin- and thrombolytic effects of streptokinase, the plasmin-streptokinase complex and the acylated derivatives of the complex with various rates of reactivation. It was established that the acylated derivatives of the plasmin-streptokinase complex possess greater stability in the blood flow and lead to more prolonged stimulation of fibrinolysis at less magnitude of its systemic activation. Due to this the acylated derivatives of the plasmin-streptokinase complex produce less pronounced fibrinogenolysis. In connection with a high affinity to fibrin their thrombolytic action does not depend on the systemic activation of fibrinolysis.

Animals↗

[The stimulation of fibrinolysis during cholinergic vasodilating reactions].

Changes in the fibrinolytic activity of blood flowing from the skeletal muscles during electrostimulation of the peripheral end of the cut-off sympathetic chain at the blockade of alpha-adrenoceptors have been studied in the acute experiments on cats. It is stated, that this action induces not only an increase of vascular conductivity but also fibrinolysis stimulation relating to the secretion of plasminogen activators to the blood. The effect of fibrinolysis stimulation was reproduced during intraarterial infusion of acetylcholine and was blocked by atropine. The vasodilating reactions on sodium nitroprusside and papaverine similar by intensity to the cholinergic reactions induce no plasminogen activator release. The existence of the specific regulation mechanism of plasminogen activator secretion, mediated by M-cholinoceptors is suggested.

Animals↗

[The antithrombotic action of a protein C activator from the venom of Agkistrodon blomhoffi ussuriensis in thrombus formation in an extracorporeal shunt in rats].

An antithrombotic action of the protein C (PC) activator from the venom of Agkistrodon blomhoffi ussuriensis on the model of platelet-dependent thrombosis in the arteriovenous shunt in rats was under investigation. Administration of the PC activator to rats resulted in a dose-dependent prolongation of the thrombus formation time, in a decrease in PC and factor V levels in blood and in APTT prolongation. There were no changes in the tissue-type plasminogen activator level and in the ADP- or epinephrine-induced platelet aggregation, but platelet adhesion to glass decreased. The possible mechanism of the antithrombotic action of the PC activator appeared to be the factor V inactivation mediated by protein C activation and the decrease in platelet adhesion.

Agkistrodon↗

[The effect of the joint administration of heparin and chitosan sulfate ether on hemostatic function].

We studied anticoagulant effects of combined administration of heparin (H) and chitosan sulfate ether (CS) (specific activity 20 UE/mg) in the ratio 1 : 1. CS enhanced anticoagulant activity of heparin in rabbits by a factor of 1.95 +/- 0.15. The intravenous injection of the mixture in a dose of 0.5 mg(H)/kg + 0.5 mg(CS)/kg and heparin injection in a dose of 1mg/kg induced the same effect. Haemorrhagic effect of this mixture was less pronounced compared to heparin, anticoagulant and antithrombotic activities remained the same. The mixture was found to decrease a number of platelets, however, this was also less pronounced compared to heparin. Thus, the use of the mixture CS + H (1 : 1) instead of double heparin dose resulted in the same effect.

Animals↗

[The vasomotor effects of the enzymes of the fibrinolytic system in rats].

Human plasmin (Pm) caused a rapid dose-dependent relaxation of norepinephrine-preconstricted isolated aortic ring and vascular net in the Wistar rat hindlimbs. Neither atropine, nor obsidan or indomethacin suppressed the Pm-induced vasodilatation of the aortic ring. Mechanical removal of endothelium and NO-blocker N-Nitro-L-Arg almost completely abolished the Pm-induced relaxation. DIP-Pm, AN-Pm and Glu-plasminogen did not change the vascular tone of the preconstricted rings. Both aprotinin and E-aminocapronic acid inhibited the relaxing effect of the Pm. Besides the circulating Pm, the enzyme forming on the endothelial surface from plasminogen under the action of urokinase, produced the vascular dilatation as well.

Animals↗