[The ability of low-molecular heparin (Fraxiparin) to overcome the action of exogenous coagulases--a fundamental difference from nonfractionated heparin]. / Sposobnost' nizkomolekuliarnogo geparina (fraksiparina) preodolevat' deistvie ékzogennykh koagulaz--fundamental'noe otlichie ot nefraktsionirovannogo geparina.

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. The experiments demonstrated that Fraxiparin the action of Echis carinatus prothrombin-activating venom to a greater degree and Agkistrodon halys halys thrombin-like coagulase to a lesser degree. Unlike the unfractionated heparin, Fraxiparan also prevents the death of white rats from acute toxic hemocoagulant shock caused by the intravenous injection of DL100 Echis carinatus venom.

[Effect of heparin on erythrocyte damage in various toxicogenic DIC syndromes]. / Vliianie heparina na povrezhdenie éritrotsitov pri razlichnykh toksikogennykh DVS-sindromakh.

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]. / Vliianie geparina na fibrinoobrazovanie pri éksperimental'nom toksogennom sindrome disseminirovannogo vnutrisosudistogo svertyvaniia krovi.

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. Besides, the effect of polymerization inhibition was revealed in the plasma of such animals.