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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">sibmed</journal-id><journal-title-group><journal-title xml:lang="ru">Сибирский научный медицинский журнал</journal-title><trans-title-group xml:lang="en"><trans-title>Сибирский научный медицинский журнал</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">2410-2512</issn><issn pub-type="epub">2410-2520</issn><publisher><publisher-name>ИЦиГ СО РАН</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.18699/SSMJ20220304</article-id><article-id custom-type="elpub" pub-id-type="custom">sibmed-802</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>МЕДИКО-БИОЛОГИЧЕСКИЕ НАУКИ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>BIOMEDICINE</subject></subj-group></article-categories><title-group><article-title>Влияние триметазидина на энергетический баланс миокарда при химиотерапии доксорубицином и циклофосфамидом</article-title><trans-title-group xml:lang="en"><trans-title>Influence of trimetazidine on myocardium energy balance during chemotherapy with doxorubicin and cyclophosphamide</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>Авагимян</surname><given-names>А. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Avagimyan</surname><given-names>A. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Ашот Арманович Авагимян</p><p>0025, г. Ереван, ул. Корюна, 2а</p><p>117418, г. Москва, ул. Цюрупы, 3</p></bio><bio xml:lang="en"><p>Ashot A. Avagimyan</p><p>0025, Yerevan, Koryun str., 2a</p><p>117418, Moscow, Tsyurupа str., 3</p></bio><email xlink:type="simple">Avagimyan.cardiology@mail.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Ереванский государственный медицинский университет им. Мх. Гераци; Научно-исследовательский институт морфологии человека им. А.П. Авцына</institution><country>Армения</country></aff><aff xml:lang="en"><institution>Yerevan State Medical University Mh. Heratsi Republic of Armenia; A.P. Avtsyn Research Institute of Human Morphology</institution><country>Armenia</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2022</year></pub-date><pub-date pub-type="epub"><day>27</day><month>06</month><year>2022</year></pub-date><volume>42</volume><issue>3</issue><elocation-id>41–46</elocation-id><permissions><copyright-statement>Copyright &amp;#x00A9; Авагимян А.А., 2022</copyright-statement><copyright-year>2022</copyright-year><copyright-holder xml:lang="ru">Авагимян А.А.</copyright-holder><copyright-holder xml:lang="en">Avagimyan A.A.</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://sibmed.elpub.ru/jour/article/view/802">https://sibmed.elpub.ru/jour/article/view/802</self-uri><abstract><p>Цель работы – проведение оценки степени ишемии миокарда крыс на хронической in vivo модели кардиотоксичности АС-режима химиотерапии с одновременным изучением обоснования применения триметазидина. Материал и методы. Объект исследования – 120 самцов инбредных крыс линии Wistar, рандомно разделенных на четыре равновеликие группы: группа 1 – контроль (введение 0,9%-го раствора хлорида натрия 3 раза в неделю); группа 2 – моделирование АС-режима химиотерапии путем внутрибрюшинного введения доксорубицина гидрохлорида в разовой дозе 2,5 мг/кг и циклофосфамида моногидрата в разовой дозе 25 мг/кг 3 раза в неделю; группа 3 – моделирование АС-режима химиотерапии с дополнительным введением триметазидина дигидрохлорида ежедневно внутрижелудочно в разовой дозе 3,0 мг/кг; группа 4 – введение триметазидина дигидрохлорида. Исследование проводили в течение двух недель. Для оценки изменений был использован микроскоп Olympus IX51. Окраска проводилась методом ГОФП (гематоксилин + основной фуксин + пикриновая кислота). Результаты и их обсуждение. В группе 2 на фоне AC-режима химиотерапии уровень фуксинофилии ткани миокарда на 87,2 и 90,9 % больше (p &lt; 0,05), чем в группах 1 и 4 соответственно, удельная площадь повреждения – на 170,8 и 167,5 % соответственно (p &lt; 0,05). В группе 3 выраженность фуксинофилии и удельная площадь повреждения миокарда статистически значимо меньше (на 26,3 и 36,5 %, p &lt; 0,05), чем в группе 2. Заключение. Триметазидин является патогенетически эффективным препаратом, предохраняющим миокард от повреждения, ассоциированного АС-режимом химиотерапии.</p></abstract><trans-abstract xml:lang="en"><p>Aim of the study was to assess the degree of myocardial ischemia in rats on chronic in vivo model, with a simultaneous assessment of justification for the use of trimetazidine. Material and methods. The object of the study was 120 male inbred Wistar rats, randomly divided into 4 equal groups: group 1 – control (administration of 0.9% sodium chloride solution 3 times a week); group 2 – simulation of the AC chemotherapy regimen by intraperitoneal administration of doxorubicin hydrochloride at a single dose of 2.5 mg/kg and cyclophosphamide monohydrate at a single dose of 25 mg/kg 3 times a week; group 3 – simulation of the AC chemotherapy regimen with additional administration of trimetazidine dihydrochloride daily by intragastric gavage at a single dose of 3.0 mg/kg; group 4 – administration of trimetazidine dihydrochloride. The study has been carried out for two weeks. An Olympus IX51 microscope was used to assess the changes. Staining was carried out by the HBFP method (hematoxylin + basic fuchsin + picronic acid). Results and discussion. In group 2, on the background of AC chemotherapy, the level of fuchsinophilia in myocardial tissue was 87.2 and 90.9 % higher (p &lt; 0.05) than in groups 1 and 4, respectively, the specific area of damage was 170.8 and 167. 5 %, respectively (p &lt; 0.05). In group 3, the severity of fuchsinophilia and the specific area of myocardial damage were statistically significantly less (by 26.3 and 36.5 %, p &lt; 0.05) than in group 2. Conclusions. Trimetazidine is a pathogenetically effective drug that protects the myocardium from damage associated with AC chemotherapy.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>доксорубицин</kwd><kwd>циклофосфамид</kwd><kwd>кардиотоксичность</kwd><kwd>химиотерапия</kwd><kwd>кардиоонкология</kwd></kwd-group><kwd-group xml:lang="en"><kwd>doxorubicin</kwd><kwd>cyclophosphamide</kwd><kwd>cardiotoxicity</kwd><kwd>chemotherapy</kwd><kwd>cardio-oncology</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">Avagimyan A., Kakturskiy L., Heshmat-Ghahdarijani K., Pogosova N., Sarrafzadegan N. Anthracycline associated disturbances of cardiovascular homeostasis. Curr. Probl. Cardiol. 2021;47(5):100909. doi: 10.1016/j.cpcardiol.2021.100909</mixed-citation><mixed-citation xml:lang="en">Avagimyan A., Kakturskiy L., Heshmat-Ghahdarijani K., Pogosova N., Sarrafzadegan N. 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