[The ability of low-molecular heparin (Fraxiparin) to overcome the action of exogenous coagulases--a fundamental difference from nonfractionated heparin].

A new previously unknown activity of the low molecular-weight heparin Fraxiparin (Sanofi) has been discovered. This is its ability to reduce the plasma clotting action of snake venom coagulases at final concentration of more than 12.5 anti-Xa U/ml, while the unfractionated heparin does not possess this property.

[Effect of heparin on erythrocyte damage in various toxicogenic DIC syndromes].

In experiments in vitro it has been established that heparin does not have a direct hemolyzing action, but it significantly reduces red blood cell resistance to acid. In experiments in vivo heparin significantly intensifies red blood cell resistance to the action of acid hemolytics. Hemolysis during intoxication with the toxins studied is, to a greater extent, secondary in relation to the intravascular blood coagulation.

[Effect of heparin on fibrinogen formation during experimental toxic syndrome of disseminated intravascular coagulation].

The formation of circulation components of fibrinogen pool in toxigenic syndrome of disseminated intravascular blood coagulation (DBC-syndrome) caused by the Vipera lebetina turanica venom has been examined by the gel-filtration method. Simultaneously it has been studied what components of fibrinogen pool are removed in paracoagulation tests and with addition of the coagulating enzymes (thrombin, reptilase and the Echis multisguamatus venom) to the plasma. The preliminary heparinization of animals poisoned by Vipera lebetina turanica venom was found to prevent the fibrinogen formation mainly at the fibrin-monomer formation stage.