TY - JOUR AU - Semenenko, S.I. AU - Semenenko, A.I. AU - Semenenko, І.F. PY - 2019/10/30 Y2 - 2024/03/29 TI - Effect of amantadine sulfate on cerebral and central hemodynamics in experimental traumatic brain injury JF - EMERGENCY MEDICINE JA - ЕМ VL - IS - 6.101 SE - Original Researches DO - 10.22141/2224-0586.6.101.2019.179607 UR - https://emergency.zaslavsky.com.ua/index.php/journal/article/view/1157 SP - 106-110 AB - <p><strong><em>Background.</em></strong> Among the leading mechanisms of the protective action of certain drugs, which are used to treat traumatic brain injury (TBI), the leading place belongs to the ability of drugs to improve cerebral circulation without suppressing regional and central hemodynamics. Purpose: to characterize the effect of amantadine sulfate and 0.9% NaCl solution on the state of cerebral and central hemodynamics in rats with acute traumatic brain injury. <strong><em>Materials and methods. </em></strong>Studies were conducted on male rats. An experimental model of severe TBI was created using a pneumatic gun. The therapeutic effect of amantadine sulfate in TBI was evaluated at a dose of 5 mg/kg twice a day for 8 days. As the drug for the control group, 0.9% NaCl was used at a dose of 2 ml/kg. To determine the efficacy of the studied drugs in TBI, the cerebral blood flow rate, blood pressure and central venous pressure were used. <strong><em>Results.</em></strong> Comparative analysis of the effectiveness of amantadine sulfate on days 4 and 8 of observation showed significantly better restoration of cerebral blood flow rate in amantadine sulfate group compared to the controls: 62.7 and 30.6 %, respectively (p &lt; 0.05). In the group of amantadine sulfate, a relatively stable decrease in blood pressure was observed during the entire observation period, from 1 to 8 days. This indicator was reduced by 21–25 % compared to baseline, but it was significantly higher than that in the control group (p &lt; 0.05). The amantadine sulfate group had significantly better central venous pressure levels compared to the control group, but at the same time, the level of the studied indicator was significantly lower than in the group of pseudo-operated animals during all periods of observation (p &lt; 0.05). <strong><em>Conclusions.</em></strong> One of the pathogenetic mechanisms of the protective action on the brain in TBI is the ability of amantadine sulfate to maintain a sufficient level of blood supply to the brain by leveling the manifestations of systemic hypotension in severe cerebral injury.</p> ER -