The antithrombotic effect of modified sulfated polysaccharides on a model of thromboplastin-induced thrombosis was investigated, which made it possible to evaluate the effectiveness of sulfated polysaccharides as a direct anticoagulant that increases the tolerance of animals to effects causing intravascular thrombosis.

Experimental studies and analyses of new compounds with different mechanisms of action on systemic haemostasis are relevant for the identification and development of potential pharmacological preparations. The modified sulphated polysaccharides with anticoagulant and antithrombin activity were studied for haemostasis. Platelet-rich plasma was obtained by centrifugation at 200g for 10 minutes. The remaining citrate blood was further centrifuged at 1500g for 10 min to obtain platelet-poor plasma. The antithrombin activity of the compounds was evaluated In vitro by their effect on the recalcification time, thrombin and prothrombin time of rabbit and human blood plasma stabilized with a 3.8% sodium citrate solution in the ratio 9:1. The results showed that the anticoagulant activity of the studied sulphates increased with an increasing degree of sulphation. Sulphated polysaccharides showed strong anticoagulant activity In vitro. The experimental results showed a significant increase in the coagulation time of blood plasma in tests for prothrombin and thrombin time. These properties of these components are of particular interest, and further detailed studies of the physicochemical characteristics and mechanisms of action of these molecules should be performed, which will eventually allow them to be used as heparin-like drugs.

Modeling of sharp alcoholic intoxication induced animal 6 mg/kg of 50-70% ethanol by introduction. On this background studied effects of N-metilsitizin alkaloids and a desoxypeganin on ADP-induced aggregation of platelets and level of intracellular Ca 2+ in the synaptosomes of a brain of rats. The obtained data render that the inhibiting effect of N-metilsitizin alkaloids and a desoxypeganin on ADP-induced aggregation of platelets is connected with oppression of a gain of cytoplasmatic concentration of Ca 2+ from depot of platelets. Thus, N-metiltsitizin alkaloids and desoxypeganin block a gain of level of intracellular Ca 2+ at the expense of increase in Ca 2+ EPR pool, provoked by ethanol.N-metiltsitizin doesn't compete with a glutamate for a binding site. Perhaps, action of Nmetiltsitizin is caused by interaction with ionic channels of NMDA receptors. The neuronal of the receptors involved in the mechanisms which are the cornerstone of AAS (including convulsive attacks) and effectively to stop to possibility of application of N-metilsitizin in regulation of dihydropyridine-sensitive calcic channels of the main subtypes them. It is shown that the possible 156 competition between desoxypeganin and a glutamate for a site of binding of regulation of opening of ionic channels. Desoxypeganin directly doesn't affect calcic canals of a NMDA receptor. Perhaps, desoxypeganin like a glutamate causes overexcitation of NMDA receptors.