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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">actabiomedica</journal-id><journal-title-group><journal-title xml:lang="ru">Acta Biomedica Scientifica</journal-title><trans-title-group xml:lang="en"><trans-title>Acta Biomedica Scientifica</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">2541-9420</issn><issn pub-type="epub">2587-9596</issn><publisher><publisher-name>Scientific Centre for Family Health and Human Reproduction Problems</publisher-name></publisher></journal-meta><article-meta><article-id custom-type="elpub" pub-id-type="custom">actabiomedica-1476</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>НАУЧНЫЕ ОБЗОРЫ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>SCIENTIFIC REVIEWS</subject></subj-group></article-categories><title-group><article-title>ПРЕКОНДИЦИОНИРОВАНИЕ КАК ЗАЩИТА ОТ ИШЕМИЧЕСКОГО ПОВРЕЖДЕНИЯ МИОКАРДА</article-title><trans-title-group xml:lang="en"><trans-title>PRECONDITIONING AS PROTECTION AGAINST ISCHEMIC MYOCARDIAL INJURY</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>Шурыгин</surname><given-names>М. Г.</given-names></name><name name-style="western" xml:lang="en"><surname>Shurygin</surname><given-names>M. G.</given-names></name></name-alternatives><email xlink:type="simple">noemail@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>Шурыгина</surname><given-names>И. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Shurygina</surname><given-names>I. A.</given-names></name></name-alternatives><email xlink:type="simple">noemail@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>Дремина</surname><given-names>Н. Н.</given-names></name><name name-style="western" xml:lang="en"><surname>Dremina</surname><given-names>N. N.</given-names></name></name-alternatives><email xlink:type="simple">noemail@neicon.ru</email><xref ref-type="aff" rid="aff-2"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Каня</surname><given-names>О. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Kanya</surname><given-names>O. V.</given-names></name></name-alternatives><email xlink:type="simple">noemail@neicon.ru</email><xref ref-type="aff" rid="aff-2"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>ФГБУ «Научный центр реконструктивной и восстановительной хирургии» СО РАМН; ФГБУН Иркутский научный центр СО РАН</institution></aff><aff xml:lang="en"><institution>Scientific Center of Reconstructive and Restorative Surgery SB RAMS; Irkutsk Scientific Center of the SB Russian Academy of Sciences</institution></aff></aff-alternatives><aff-alternatives id="aff-2"><aff xml:lang="ru"><institution>ФГБУ «Научный центр реконструктивной и восстановительной хирургии» СО РАМН</institution></aff><aff xml:lang="en"><institution>Scientific Center of Reconstructive and Restorative Surgery SB RAMS</institution></aff></aff-alternatives><pub-date pub-type="collection"><year>2013</year></pub-date><pub-date pub-type="epub"><day>28</day><month>04</month><year>2013</year></pub-date><volume>0</volume><issue>2(2)</issue><fpage>206</fpage><lpage>210</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Шурыгин М.Г., Шурыгина И.А., Дремина Н.Н., Каня О.В., 2013</copyright-statement><copyright-year>2013</copyright-year><copyright-holder xml:lang="ru">Шурыгин М.Г., Шурыгина И.А., Дремина Н.Н., Каня О.В.</copyright-holder><copyright-holder xml:lang="en">Shurygin M.G., Shurygina I.A., Dremina N.N., Kanya O.V.</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.actabiomedica.ru/jour/article/view/1476">https://www.actabiomedica.ru/jour/article/view/1476</self-uri><abstract><p>В статье обсуждается феномен метаболической адаптации к ишемии после повторяющихся кратковременных эпизодов снижения перфузии миокарда. Показано, что феномен ишемического прекондиционирования заключается в существенном повышении устойчивости ткани к ишемическому и реперфузионному повреждению, возникающему после нескольких коротких эпизодов ишемии-реперфузии. При этом ишемическое прекондиционирование является многофакторным явлением, реализуемым как через адаптацию внутриклеточных каскадов к изменениям метаболических условий, так и структурной перестройкой миокарда с повышением его толерантности к снижению перфузии. Использование внешних воздействий, направленных на отдельные звенья этого процесса или их совокупность, позволит улучшить исходы ишемических эпизодов и сохранение функции миокарда при компрометированном сосудистом русле. Особо подчеркнуто, что одним из значимых стимулов ишемического прекондиционирования могут выступать факторы роста - FGF2 и VEGF. При этом защитный эффект реализуется как путем повышения жизнеспособности клеток сократительного миокарда и эндотелиоцитов сосудов миокарда в очаге ишемического повреждения, так и за счет неоангиогенеза и повышения регенераторной способности зрелых кардиомиоцитов</p></abstract><trans-abstract xml:lang="en"><p>The article discusses the phenomenon of metabolic adaptation to ischemia after repeated episodes of transient reduction in myocardial perfusion. It is shown that the phenomenon of ischemic preconditioning is to significantly improve the stability of the ischemic tissue and reperfusion injury that occurs after a few brief episodes of ischemia-reperfusion. Thus ischemic preconditioning is a multifactorial phenomenon, as implemented through adaptation to changes in the intracellular cascade of metabolic conditions and the restructuring of the myocardium with increased tolerance to its lower perfusion. The use of external actions aimed at the individual links of the process or set of them, will improve the outcomes of ischemic episodes, and better preservation of myocardial function in a compromised vascular bed. It is shown that one of the major incentives of ischemic preconditioning may make growth factors - FGF2 and VEGF. In this case, the protective effect is realized as by increasing the viability of myocardial contractile cells and vascular endothelial cells in myocardial ischemic damage of the hearth, and by neo-angiogenesis and improve the regenerative ability of mature cardiomyocytes.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>ишемия</kwd><kwd>прекондиционирование</kwd><kwd>факторы роста</kwd></kwd-group><kwd-group xml:lang="en"><kwd>FGF2</kwd><kwd>VEGF</kwd><kwd>ischemia preconditioning</kwd><kwd>growth factors</kwd><kwd>FGF2</kwd><kwd>VEGF</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">Влияние эндотелиального фактора роста на постинфарктное ремоделирование миокарда крыс / Н.Н. 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