EFFECTIVENESS OF CORRECTION OF DISCUSSION OF CARBOHYDRATE METABOLISM IN RATS WITH CRANIOCEREBRAL INJURY
The development and introduction into practice of emergency neurology of new drugs capable of influencing secondary neuronal damage in patients with traumatic brain injury (TBI) has made a significant impact on the recovery of such patients.
Aim of the work was to evaluate the magnitude of cerebroprotective action of amantadine sulfate in terms of impaired carbohydrate metabolism of the brain against the background of experimental TBI.
Materials and methods. The experimental model of severe TBI was caused by the action of a carbon dioxide flow under pressure, which was created using a gas balloon of pneumatic gun. The therapeutic effect of amantadine sulfate on TBI model was evaluated with a 5 mg/kg dose. The pseudo-operated animals and control group received 0.9 % NaCl solution at a dose of 2 ml/kg with IV administration.
Results. The obtained results confirm the formation of a hypo-energetic state in the brain cells of rats on the background of TBI, which is probably a consequence of the suppression of the processes of oxidative phosphorylation and its conjugation with tissue respiration. TBI is accompanied by activation of anaerobic glycolysis and inhibition of aerobic glucose oxidation, proving that there is an imbalance between the levels of lactate and pyruvate intermediates. 8-day infusion of rats with traumatic brain injury of amantadine sulfate, inhibited anaerobic glycolysis hyperactivation, stimulated tissue respiration processes, reduced signs of lactic acidosis and development of secondary alteration of brain cells by non-oxidized products.
Conclusions. In the course of the experiment, it was found that the treatment of rats, with TBI model, with 0.9 % NaCl solution did not significantly contribute to the restoration of impaired energy metabolism (p<0.05) and did not reduce the manifestation of metabolic acidosis in the damaged brain (p<0.05). The use of amantadine sulphate in TBI rats significantly corrects carbohydrate metabolism disorders than 0.9 % NaCl solution and contributes to the reduction of metabolic acidosis in the damaged brain (p<0.05).
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