острая кровопотеря, клиническая смерть, реанимация, головной мозг, метаболизм, Medicine

In the course of experiments in 210 white mongrel male rats, endured 5-min clinical death from acute blood loss the mechanisms of energy, carbohydrate, lipid metabolism disturbance in postresuscitated brain tissue have been studied. It has been established that primary and secondary hypoxia, metabolic acidosis, excessive lipid peroxidation process activity, endotoxemia, neuron overload by Ca ions appeared to be the principle pathogenetic factors of the abovementioned disturbances. Pathogenetic block-scheme of early postresuscitation metabolic disturbances in brain was presented. The validity of this block-scheme principle theses was demonstrated by means of gutimin antihypoxanths (50 mg/kg) and sodium γ-hydroxybutyrate (300 mg/kg), ionolantioxidant (100 mg/kg), slow isoptin Ca-canals blocker (0,1 mg/kg) injected before clinical death.