The possibilities of pharmacological correction of the disturbance of carbohydrate metabolism in brain rates with traumatic brain injury
The development and introduction into practice of emergency neurology of new drugs capable of influencing the secondary damage of neurons in patients with traumatic brain injury (TBI) has significantly affected the recovery of such patients. The aim of the study was to evaluate the magnitude of the cerebroprotective effect of amantadine sulfate on the index of impaired carbohydrate metabolism of the brain against the background of experimental TBI. The experimental TBI model of severe severity was caused by the action of a carbon dioxide flow under pressure created using a gas balloon pneumatic gun. The therapeutic effect of amantadine sulfate on model TBI was evaluated using a dose of 10 mg/kg. The pseudoperated animals and control group received 0.9% NaCl solution at a dose of 2 ml/kg i/v. The obtained results were processed by the method of variational statistics using Student's t-test, changes of indicators were considered probable at p≤0.05. In the course of the experiment, it was found that the treatment of rats with model TBI 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 sulfate in TBI rats significantly better 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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