Morphofunctional Characteristic of Edema-Swelling of the Cerebral Cortex of White Rats After Severe Traumatic Brain Injury Without the Use of L-Lysine Escinate and Against the Background of Its Use
https://doi.org/10.23934/2223-9022-2020-9-2-251-258
Abstract
Aim of study The study is devoted to a morphometric assessment of the manifestations of edema-swelling of the somatosensory cortex (SSC) of the brain of white rats after severe traumatic brain injury (TBI) without using L-lysine escinate and when using it as a therapeutic effect.
Material and methods We stained sections with hematoxylin-eosin and performed morphometric methods. On thin (4 μm) serial frontal sections of SSC, neurons and microvessels in the control (intact animals, n=5) were examined in 1 (n= 5), 3 (n=5), 5 (n=5), 7 (n=5) and 14 (n=5) days after injury without treatment (n=25, comparison group) and with treatment (n=25, main group). In color raster images (lens x100), using the plug-in filter “Find Maxima”, maximum brightness areas (MBA) were determined , which were then analyzed using the “Analyze Particles” program from ImageJ 1.52 s. MBA corresponded to SSC sites with a high degree of hydration of nerve tissue - edema-swelling. Statistical hypotheses were tested using nonparametric criteria.
Results and discussion In control animals, a low degree of hydration of SSC tissue was noted (relative area 3-8%). In the comparison group, 1 and 3 days after STBI, foci of edema-swelling covered up to 30% of SSC, in 5 days - up to 15%, in 7 days - up to 20%, in 15 - up to 18%. Significant heteromorphism and heterogeneity of changes in the neuropil around neurons and blood vessels was noted. In the dynamics of the post-traumatic period, the proportion of large foci of edema-swelling (intra- and perineuronal, perivascular) decreased. In the main group, one day after STBI, there was a statistically significantly smaller number of foci of edema-swelling and their total relative area. The values range of these variables significantly decreased. L-lysine escinat affected the water balance most effectively in the acute post-traumatic period (day 1 and 3). The drug “smoothed out” the manifestation peaks (number, focal area) of edema-swelling: the values of the studied morphometric indicators were statistically significantly different. Consequently, morphometric signs of hydropic dystrophy after STBI were detected in both studied groups during the 15 days of observation.
Conclusion The degree of SSC nervous tissue hydration increased after STBI. L-lysine escinate statistically significantly reduced manifestations of hydropic dystrophy. The drug significantly affected the degree of hydration of neural tissue observed in the early post-traumatic period.
Keywords
About the Authors
I. P. KoshmanRussian Federation
Full-time graduate student of the Department of Neurology and Neurosurgery
12 Lenina St., Omsk 644099
S. S. Stepanov
Russian Federation
Doctor of Medical Sciences, Senior Researcher, Department of Histology, Cytology and Embryology, Federal State Budgetary Educational Institution of Higher Education
12 Lenina St., Omsk 644099
A. Y. Shoronova
Russian Federation
Assistant, Department of Histology, Cytology and Embryology, Federal State Budgetary Educational Institution of Higher Education
12 Lenina St., Omsk 644099
A. G. Kalinichev
Russian Federation
Doctor of Medical Sciences, Professor of the Department of Neurology and Neurosurgery
12 Lenina St., Omsk 644099
V. A. Akulinin
Russian Federation
Doctor of Medical Sciences, Professor, Head of the Department of Histology, Cytology and Embryology
12 Lenina St., Omsk 644099
D. B. Avdeyev
Russian Federation
Candidate of Veterinary Sciences, Senior Lecturer, Department of Histology, Cytology and Embryology, Federal State
Budgetary Educational Institution of Higher Education
12 Lenina St., Omsk 644099
V. I. Sergeyev
Russian Federation
3rd year student of the Faculty of Dentistry, Federal State Budgetary Educational Institution of Higher Education
12 Lenina St., Omsk 644099
References
1. Akhanov GZh, Dyusembekov EK, Nurbakyt AN. Clinical and epidemiological aspects of an isolated craniocerebral trauma. Neurosurgery and Neurology of Kazakhstan. 2017;2(47):65–71. (In Russ).
2. Likhterman LB. Cherepno-mozgovaya travma. Diagnostika i lechenie. Moscow; GEOTAR-Media Publ., 2014. (In Russ).
3. Krylov VV, Konovalov AN, Dash’yan VG, Kondakov EN, Tanyashin SV, Gorelyshev SK, et al. Neurosurgery in Russian Federation. Burdenko’s Journal of Neurosurgery. 2017; 1(81):5–12. (In Russ).
4. Hackenberg K, Unterberg A. Schädel-Hirn-Trauma [Traumatic brain injury]. Nervenarzt. 2016; 87(2):203–216. (in German). PMID: 26810405. PMID: 26810405 https://doi.org/10.1007/s00115-015-0051-3
5. Zadvornov AA, Golomidov AV, Grigor’ev EV. Clinical pathophysiology of cerebral edema (part 2). Messenger of Anesthesiology and Resuscitation. 2017;14(4):52–60. (In Russ).
6. Krylov VV, Petrikov SS, Solodov AA. Vnutricherepnaya gipertenziya. Moscow: BINOM Publ.; 2016. (In Russ).
7. Latysheva VY, Kurman VI, Tsukanov AN, Usova NN, Galinovskaya NV, Olizarovich MV. Otek golovnogo mozga: etiopatogenez, klinika, diagnostika, lechenie. Gomel’; 2016. (In Russ).
8. Petrikov SS, Solodov AA, Badygov SA, Mekhia Mekhia ED, Krylov VV. The effect of L-lysine of escinate on intracranial pressure in patients with severe traumatic brain injury who are in critical condition. Russian Sklifosovsky Journal Emergency Medical Care. 2016; 2:31–36. (In Russ).
9. Mirzabaev MZh, Djusembekov EK, Aliev MA. Dynamics and correction ways of intracranial pressure in patients with heavy brain injury. Herald of Almaty State Institute of Advanced Education. 2017;3:42–27. (In Russ).
10. Schwarzmaier SM, Gallozzi M, Plesnila N. Identification of the Vascular Source of Vasogenic Brain Edema following Traumatic Brain Injury Using In Vivo 2-Photon Microscopy in Mice. J Neurotrauma. 2015;32(13):990–1000. PMID: 25585052 https://doi.org/10.1089/neu.2014.3775
11. Zadvornov AA, Golomidov AV, Grigor’ev EV. Clinical pathophysiology of cerebral edema (Part 1). Messenger of Anesthesiology and Resuscitation. 2017;14(3):44–50. (In Russ). https://doi.org/10.21292/2078-5658-2017-14-3-44-50
12. Stokum JA, Gerzanich V, Simard JM. Molecular pathophysiology of cerebral edema. J Cereb Blood Flow Metab. 2016;36(3):513–538. PMID: 26661240 https://doi.org/10.1177/0271678x15617172
13. Ng SY, Lee AYW. Traumatic Brain Injuries: Pathophysiology and Potential Therapeutic Targets. Front Cell Neurosci. 2019;13:528. PMID: 31827423. https://doi.org/10.3389/fncel.2019.00528
14. Parfenov VA. The use of L-lysine of escinate in diseases of the central nervous system. Neurology, Neuropsychiatry, Psychosomatics. 2011;3(4):99–104. (In Russ).
15. Badalov VI, Shevelev PYu, Reva VA, Semenov EA, Adzhieva ZN, Mikhailovskaya EM, et al. Development of an experimental model of severe traumatic brain injury. Voenno-medicinskij zhurnal. 2018; 339(7):15–21. (In Russ).
16. Paxinos G, Watson C. The Rat Brain in Stereotaxic Coordinates. The New coronal set. 5th ed. San Diego: Elsevier Academic Press; 2005.
17. Borovikov V. Statistica. Iskusstvo analiza dannykh na komp’yutere. 2nd ed. Saint Petersburg: Piter Publ.; 2003. (In Russ).
Review
For citations:
Koshman I.P., Stepanov S.S., Shoronova A.Y., Kalinichev A.G., Akulinin V.A., Avdeyev D.B., Sergeyev V.I. Morphofunctional Characteristic of Edema-Swelling of the Cerebral Cortex of White Rats After Severe Traumatic Brain Injury Without the Use of L-Lysine Escinate and Against the Background of Its Use. Russian Sklifosovsky Journal "Emergency Medical Care". 2020;9(2):251-258. https://doi.org/10.23934/2223-9022-2020-9-2-251-258