Comparison of Hemostatic and Neuro Protector Properties of Alkaloids N-Metiltsitizin and a Desoxypeganin in the Conditions of in Vitro
Annotatsiya
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 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.
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