The study of metabolic processes in the brain in conditions of hemorrhagic stroke on the background of pharmacotherapy with ademol
In the article, on the model of subarachnoid hemorrhage, some biochemical aspects of the cerebroprotective effect of an industrial sample of an ampoule 1.0% solution of ademol are disclosed, namely its effect on carbohydrate and energy metabolism, the state of antioxidant systems, the activity of lipoperoxidation processes, and the functioning of the L-arginine / NO system in rat brain as possible metabolitotropic components of its protective effect on brain neurons. Severe subarachnoid hemorrhage was created under conditions of propofol anesthesia by injection of heparinized autologous blood (0.1 ml / kg volume) through a catheter located in the subarachnoid space. We used the Student t parametric criterion, W. White nonparametric criterion, Ť Wilcoxon paired criterion — to determine significant changes in the dynamics within the group. Differences were considered statistically significant at p<0.05. Using the example of the acute period of subarachnoid hemorrhage, it was established that ademol is able to eliminate brain energy deficiency (increase the content of adenosine triphosphoric acid and pyruvate in the brain while increasing the energy charge relative to the control pathology samples by an average of 45.1, 42.9 and 22.0%, p<0.05) reduce lactic acidosis (reduce the lactate content by 31.9%, p<0.05), eliminate the manifestations of oxidative stress (reduce the level of malondialdehyde and carbonyl groups of proteins on average by 30.5 and 18.8%, against the background of an increase in the activity of superoxide dismutase, glutathione peroxidase and catalase by 42.1, 25.2 and 37.6%, respectively, p<0.05), simulate the exchange of nitric monoxide (increase the activity of NO synthase with a simultaneous increase in the content of NO L-arginine donor on average by 14.0 and 44.0%, respectively, p<0.05). In these properties, ademol significantly exceeded the effectiveness of solutions of amantadine and magnesium sulfate.
2. Khodakivsʹkyy, O. A., Zhaboyedova, N. V., & Rokunetsʹ, I. L. (2016). Porivnyalʹna otsinka vplyvu Ademolu ta nimodypinu na tserebralʹnu hemodynamiku v kori holovnoho mozku [Comparative assessment of the effects of Ademol and nimodipine on cerebral hemodynamics in the cerebral cortex]. Svit medytsyny ta biolohiyi – World of Medicine and Biology, 3 (57), 150–153.
3. Chekman, I. S., Gubskiy, YU. I., & Belenichev, I. F. (2015). Doklinicheskoye izucheniye spetsificheskoy aktivnosti potentsial'nykh neyroprotektivnykh preparatov [Preclinical study of the specific activity of potential neuroprotective drugs]. Kií̈v: Ínstitut farmakologíí̈ ta toksikologíí̈ MOZ Ukraí̈ni.
4. Han, J., Yang, F., Jiang, W., Zhang, G., Liu, Z., Liu, X., & Zhao, G. (2016). Hydroxyethyl starch 130/0.4 and sodium chloride injection as adjunctive therapy in patients with cerebral hypoperfusion. BMC Neurology, 12, 127–135. doi:10.1186/1471-2377-12-127.
5. Lehmann, L., Bendel, S., Uehlinger, D.E., Takala, J., Schafer, M., Reinert, M., & Jakob, S. M. (2015). Randomized, double-blind trial of the effect of fluid composition on electrolyte, acid base, and fluid homeostasis in patients early after subarachnoid hemorrhage. Neurocritical Care, 18 (1), 5–12. doi: 10.1007/s12028-012-9764-3.
6. Li, C. Y., Karmarkar, A., Adhikari, D., Ottenbacher, K., & Kuo, Y. F. (2018). Effects of Age and Sex on Hospital Readmission in Traumatic Brain Injury. Arch. Phys. Med. Rehabil., 99 (7), 1279–1288.e1. doi: 10.1016/j.apmr.2017.12.006.
7. Oddo, M., Poole, D., Helbok, R., Meyfroidt, G., Stocchetti, N., Bouzat, P. & Citerio, G. (2018). Fluid therapy in neurointensive care patients: ESICM consensus and clinical practice recommendations. Intensive Care Medicine, 44 (4), 449–463. doi: 10.1007/ s00134-018-5086-z.
This work is licensed under a Creative Commons Attribution 4.0 International License.