[The effect of the joint administration of heparin and chitosan sulfate ether on hemostatic function]. / Vliianie sovmestnogo vvedeniia geparina i sernokislogo éfira khitozana na funktsiiu gemostaza.

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.

[The antithrombotic action of a protein C activator from the venom of Agkistrodon blomhoffi ussuriensis in thrombus formation in an extracorporeal shunt in rats]. / Antitromboticheskoe deistvie aktivatora proteina C iz iada Agkistrodon blomhoffi ussuriensis pri tromboobrazovanii v ékstrakorporal'nom shunte u krys.

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.

Role of sympathetic cholinergic pathway in the neurogenous control of tissue-type plasminogen activator release into the blood.

The changes in conductivity of skeletal muscle vessels of the hind leg and tissue-type plasminogen activator (t-PA) activity in outflowing blood after electrostimulation (5 V, 0.5 ms, 20 Hz, 30 s) at the L4-L5 level of the peripheral end of the transected isolated sympathetic chain were studied in experiments on anaesthetized cats. Stimulation of the sympathetic chain induced vasoconstriction and release of t-PA from the vascular wall into the blood. Pretreatment with the beta-adrenoblocker propranolol neither changed the character of vascular reactions nor blocked t-PA secretion. Efferent stimulation of the sympathetic chain against a background of alpha-adrenoceptor blockade by dihydroergotoxin increased blood flow and was accompanied by a rise in t-PA activity. The M-cholinergic blocker atropine suppressed both vascular relaxation and release of t-PA into the blood. Vasodilatation accompanied by t-PA secretion could be induced by intraarterial infusion of acetylcholine and blocked by atropine. The existence of a neurogenic mechanism controlling t-PA release from the vascular wall involving a sympathetic cholinergic pathway and connected with excitation of vascular M-cholinoceptors by acetylcholine is suggested.

[The thrombolytic activity of acylated activator complexes of plasmin-streptokinase with different rates of reactivation]. / Tromboliticheskaia aktivnost' atsilirovannykh aktivatornykh kompleksov plazmin--streptokinaza s razlichnymi skorostiami reaktivatsii.

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.

[The stimulation of fibrinolysis during cholinergic vasodilating reactions]. / Stimuliatsiia fibrinoliza pri kholinergicheskikh sosudorasshiriaiushchikh reaktsiiakh.

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.

[Action of doxorubicin and a doxorubicin-heparin complex on the growth and metastasis of experimental tumors and the hemostatic system indices]. / Deistvie doksorubitsina i kompleksa doksorubitsin--geparin na rost i metastazirovanie éksperimental'nykh opukholei i nekotorye pokazateli sistemy gemostaza.

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.