Effect of amantadine sulfate on cerebral and central hemodynamics in experimental traumatic brain injury

Authors

  • S.I. Semenenko National Pirogov Memorial Medical University, Vinnytsia, Ukraine
  • A.I. Semenenko National Pirogov Memorial Medical University, Vinnytsia, Ukraine
  • І.F. Semenenko National Pirogov Memorial Medical University, Vinnytsia, Ukraine

DOI:

https://doi.org/10.22141/2224-0586.6.101.2019.179607

Keywords:

amantadine sulfate, cerebral hemodynamics, central hemodynamics, acute traumatic brain injury

Abstract

Background. 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. Materials and methods. 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. Results. 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 < 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 < 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 < 0.05). Conclusions. 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.

Downloads

Download data is not yet available.

References

Majdan M, Plancikova D, Brazinova A еt al. Epidemiology of traumatic brain injuries in Europe: a cross-sectional analysis. Lancet Public Health. 2016 Dec;1(2):e76-e83. doi: 10.1016/S2468-2667(16)30017-2.

Abou El Fadl MH, O'Phelan KH. Management of Traumatic Brain Injury: An Update. Neurosurg Clin N Am. 2018;29(2):213–221.

Carney N, Totten AM, O'Reilly C. Guidelines for the Management of Severe Traumatic Brain Injury 4th Edition Reviewed for evidence–based integrity and endorsed by the American Association of Neurological Surgeons and the Congress of Neurological Surgeons. September 2016/https://braintrauma.org/uploads/03/12/Guidelines for Management of Severe TBI 4th_Edition.pdf.

Gardner RC, Dams-O'Connor K, Morrissey MR, Manley GT. Geriatric Traumatic Brain Injury: Epidemiology, Outcomes, Knowledge Gaps, and Future Directions. J Neurotrauma. 2018 Feb 15. doi: 10.1089/neu.2017.5371.

Llompart-Pou JA, Pérez-Bárcena J. Geriatric traumatic brain injury: An old challenge. Med Intensiva. 2019 Jan - Feb;43(1):44-46.

Arun P, Ariyannur PS, Moffett JR et al. Metabolic acetate therapy for the treatment of traumatic brain injury. J Neurotrauma. 2010;27(1):293–298.

Hatefi M, Behzadi S, Dastjerdi MM et al. Correlation of Homocysteine with Cerebral Hemodynamic Abnormality, Endothelial Dysfunction Markers, and Cognition Impairment in Patients with Traumatic Brain Injury. World Neurosurg. 2017;97:70–79. doi: 10.1016/j.wneu.2016.09.080.

Semenenko AI, Kobelyatsky YuYu, Kondratsky BO, Semenenko IF. Features of the influence of some infusion solutions on cerebral hemodynamics in acute ischemic stroke. Emergency medicine.2016; 4(75), 118–121. (In Ukrainian).

Khodakivsky OA. Estimation of the influence of adamantane derivative (compound YUK-1) on cerebral hemodynamics in conditions of anesthesia and acute cerebral ischemia. Pathology. 2010;2:35–37. (In Ukrainian).

Talving P, Karamanos E, Teixeira PG et al. Intracranial pressure monitoring in severe head injury: compliance with Brain Trauma Foundation guidelines and effect on outcomes: a prospective study. J Neurosurg. 2013;119(5):1248–1254. doi: 10.3171/2013.7.

Farahvar A, Gerber LM, Chiu YL et al. Increased mortality in patients with severe traumatic brain injury treated without intracranial pressure monitoring. J Neurosurg. 2012;117(4):729–734. doi: 10.3171/2012.7.

Boyarinov GA, Deryugina AV, Yakovleva EI et al. Pharmacological correction of microcirculation in rats after traumatic brain injury. Cytology. 2016;8(58):610–617. (In Russian).

Semenenko AI. Assessment of the therapeutic effect of 0.9% NaCl solution according to cerebral hemodynamics in rat cerebral ischemia-reperfusion. Journal of Grodno State Medical University. 2014;3(47):49-52.

Lapach SN, Chubenko AB, Babich M. Statistical methods in biomedical research using Excel. K.: MORION, 2000:320.

Eroğlu O, Deniz T, Kisa Ü, Atasoy P, Aydinuraz K. Effect of hypothermia on apoptosis in traumatic brain injury and hemorrhagic shock model. Injury. 2017;48(12):2675–2682. doi: 10.1016/j.injury.2017.09.032.

Published

2021-10-01

How to Cite

Semenenko, S., Semenenko, A., & Semenenko І. (2021). Effect of amantadine sulfate on cerebral and central hemodynamics in experimental traumatic brain injury. EMERGENCY MEDICINE, (6.101), 106–110. https://doi.org/10.22141/2224-0586.6.101.2019.179607

Issue

Section

Original Researches

Most read articles by the same author(s)

1 2 > >>