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<article article-type="research-article" dtd-version="1.3" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xml:lang="ru"><front><journal-meta><journal-id journal-id-type="publisher-id">rmt</journal-id><journal-title-group><journal-title xml:lang="ru">Общая реаниматология</journal-title><trans-title-group xml:lang="en"><trans-title>General Reanimatology</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">1813-9779</issn><issn pub-type="epub">2411-7110</issn><publisher><publisher-name>FSBI "SRIGR" RAMS</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.15360/1813-9779-2016-4-24-36</article-id><article-id custom-type="elpub" pub-id-type="custom">rmt-1537</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="ru"><subject>ОРИГИНАЛЬНЫЕ ИССЛЕДОВАНИЯ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>ORIGINAL INVESTIGATIONS</subject></subj-group></article-categories><title-group><article-title>ТОРМОЗНЫЕ ИНТЕРНЕЙРОНЫ НЕОКОРТЕКСА ЧЕЛОВЕКА ПОСЛЕ КЛИНИЧЕСКОЙ СМЕРТИ</article-title><trans-title-group xml:lang="en"><trans-title>Inhibitory Interneurons of The Human Neocortex after Clinical Death</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Акулинин</surname><given-names>В. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Akulinin</surname><given-names>V. A.</given-names></name></name-alternatives><email xlink:type="simple">akulinin@omsk-osma.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Степанов</surname><given-names>С. С.</given-names></name><name name-style="western" xml:lang="en"><surname>Stepanov</surname><given-names>S. S.</given-names></name></name-alternatives><email xlink:type="simple">face@neicon.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Мыцик</surname><given-names>А. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Mytsik</surname><given-names>A. V.</given-names></name></name-alternatives><email xlink:type="simple">face@neicon.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Степанов</surname><given-names>А. С.</given-names></name><name name-style="western" xml:lang="en"><surname>Stepanov</surname><given-names>A. S.</given-names></name></name-alternatives><email xlink:type="simple">face@neicon.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Разумовский</surname><given-names>В. С.</given-names></name><name name-style="western" xml:lang="en"><surname>Rasumovsky</surname><given-names>V. S.</given-names></name></name-alternatives><email xlink:type="simple">face@neicon.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff xml:lang="ru" id="aff-1"><institution>Омский государственный медицинский университет Минздрава России</institution><country>Russian Federation</country></aff><pub-date pub-type="collection"><year>2016</year></pub-date><pub-date pub-type="epub"><day>26</day><month>10</month><year>2016</year></pub-date><volume>12</volume><issue>4</issue><fpage>24</fpage><lpage>36</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Акулинин В.А., Степанов С.С., Мыцик А.В., Степанов А.С., Разумовский В.С., 2016</copyright-statement><copyright-year>2016</copyright-year><copyright-holder xml:lang="ru">Акулинин В.А., Степанов С.С., Мыцик А.В., Степанов А.С., Разумовский В.С.</copyright-holder><copyright-holder xml:lang="en">Akulinin V.A., Stepanov S.S., Mytsik A.V., Stepanov A.S., Rasumovsky V.S.</copyright-holder><license xml:lang="ru" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>Данная работа распространяется под лицензией Creative Commons Attribution 4.0.</license-p></license><license xml:lang="en" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>This work is licensed under a Creative Commons Attribution 4.0 License.</license-p></license></permissions><self-uri xlink:href="https://www.reanimatology.com/rmt/article/view/1537">https://www.reanimatology.com/rmt/article/view/1537</self-uri><abstract><p>Цель: изучение количества и структуры интернейронов в разных областях коры головного мозга человека после остановки сердца (клиническая смерть).Материал и методы. Основная группа (n=7, мужчины) пациенты, пережившие  остановку сердца и умершие позже (через 7—10 и 70—90 сут) от повторной острой сердечной недостаточности. Контрольная группа (n=4, мужчины) погибшие в результате несчастных случаев. С использованием световой и конфокальноймикроскопии проведен гистологический и морфометрический анализ 420 полей зрения неокортекса (окраска по Нисслю, на кальбиндин D28k и нейропептид Y).Результаты. У умерших обеих групп подтвердили наличие в неокортексе всех главных типов интернейронов (корзинчатые, клетки Мартинотти и нейроглиаформные интернейроны), в соответствии с морфологией их тел и дендритных отростков. При этом количество кальбиндин- и NPY-позитивныхнейронов неокортекса было одинаковым в контроле и в постреанимационном периоде. Однако, поля кальбиндин- и NPY-позитивных структур, включая тела нейронов и их дендриты, были значительно больше в образцах основной группы, чем в контроле. Максимальное увеличение общей площади кальбиндин-позитивных структур наблюдалось через 90 сут после клинической смерти. Площадь NPY-по-зитивных структур была больше, чем в контроле, уже через 7 сут после оживления и осталась на этом уровне через 90 сут.Вывод. Наши находки свидетельствуют об увеличении после клинической смерти экспрессии кальбиндина и NPY в неокортексе человека, что рассматривается как компенсаторная реакция неповрежденных тормозных корковых интернейронов, направленная на защиту мозга от ишемии.</p></abstract><trans-abstract xml:lang="en"><p>Objective: to analyze the human neocortex interneurons (areas 4, 10, 17 and 21 by Brodmann) after cardiac arrest (clinical death).Materials and methods. The main group included patients (n=7, men) who survived 7—10 days and 70—90 days after cardiac arrest and later died due to heart failure. The control group (n=4, men) included individuals after sudden fatal accidents. The morphometric and histological analysis of 420 neocortical fields (Nissl#staining,calbindin D28k, neuropeptide Y) was performed using light and confocal microscopy.Results. We verified all main types of interneurons (Basket, Martinotti, and neurogliaform interneurons) in neocortex based on the morphology of their bodies and dendritic processes in both groups. The number of calbindin- and NPY-positive neurons in the neocortex was similar in the control and in the postoperative period.However, calbindin- and NPY-immunopositive structure fields including neuronal cell bodies and their dendrites were significantly more represented in neocortex of patients from the main group. Maximum increase in common square in the relative areas of calbindin-immunopositive structures was observed 90 days after ischemia. The squares of NPY#immunopositive fields became larger seven days after resuscitation and remained increased on 90th day post-resuscitation.Conclusion. Our findings demonstrate an increase of calbindin and NPY expression in human neocortex after clinical death, which can be explained by a compensatory  eaction of undamaged inhibitory cortical interneurons directed to protectbrain from ischemia.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>клиническая смерть</kwd><kwd>человек</kwd><kwd>неокортекс</kwd><kwd>тормозные интернейроны</kwd><kwd>кальбиндин D28k</kwd><kwd>нейропептид Y</kwd></kwd-group><kwd-group xml:lang="en"><kwd>clinical death</kwd><kwd>man</kwd><kwd>neocortex</kwd><kwd>inhibitory interneurons</kwd><kwd>calbindin D28k</kwd><kwd>neuropeptide Y</kwd></kwd-group></article-meta></front><back><ref-list><title>References</title><ref id="cit1"><label>1</label><citation-alternatives><mixed-citation xml:lang="ru">Аврущенко М.Ш., Острова И.В., Волков А.В. Постреанимационные изменения экспрессии глиального нейротрофического фактора (GDNF): взаимосвязь с повреждением клеток Пуркинье мозжечка (экспериментальное исследование). 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