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.

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.

Increasing amount of evidence suggests that age-related dysregulation of neuronal Ca2+ homeostasis may play a proximal role in the pathogenesis of Alzheimer's disease, as impaired Ca2+ can cause synaptic deficits and contribute to the accumulation of Aβ plaques and neurofibrillary tangles.Ca2+ disruption is known to be mostly involved in all pathologies of Alzheimer's disease, the use of chemical agents or small molecules specific for Ca2+ channels, or the treatment of proteins on the plasma membrane and intracellular organelle membranes for correction is quite possible. Neuronal dysregulation of Ca2+ may open up a new approach to the prevention and treatment of Alzheimer's disease. The article shows the possible competition between the polyphenols PС-6, PС-7 and glutamate for the area of regulation of the opening of ion channels of ionotropic NMDA-receptors in the brain of rats.