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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">cardiotomsk</journal-id><journal-title-group><journal-title xml:lang="ru">Сибирский журнал клинической и экспериментальной медицины</journal-title><trans-title-group xml:lang="en"><trans-title>Siberian Journal of Clinical and Experimental Medicine</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">2713-2927</issn><issn pub-type="epub">2713-265X</issn><publisher><publisher-name>TSU publishing</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.29001/2073-8552-2020-35-2-163-166</article-id><article-id custom-type="elpub" pub-id-type="custom">cardiotomsk-991</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>ЭКСПЕРИМЕНТАЛЬНЫЕ ИССЛЕДОВАНИЯ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>EXPERIMENTAL STUDIES</subject></subj-group></article-categories><title-group><article-title>Роль β-адренорецепторов в стресс-индуцированном повреждении сердца у крыс в модели синдрома такотсубо</article-title><trans-title-group xml:lang="en"><trans-title>The role of β-adrenergic receptors in stress-induced cardiac injury in a rat model of Takotsubo syndrome</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-9603-822X</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Курбатов</surname><given-names>Б. К.</given-names></name><name name-style="western" xml:lang="en"><surname>Kurbatov</surname><given-names>B. K.</given-names></name></name-alternatives><bio xml:lang="ru"><p>младший научный сотрудник, лаборатория экспериментальной кардиологии,</p><p>634012, Томск, ул. Киевская, 111а</p></bio><bio xml:lang="en"><p>Junior Research Scientist, Laboratory of Experimental Cardiology,</p><p>111a, Kievskaya str., Tomsk, 634012</p></bio><email xlink:type="simple">bobersanker@gmail.com</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-1991-6516</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Прокудина</surname><given-names>Е. С.</given-names></name><name name-style="western" xml:lang="en"><surname>Prokudina</surname><given-names>E. S.</given-names></name></name-alternatives><bio xml:lang="ru"><p>канд. мед. наук, научный сотрудник, лаборатория экспериментальной кардиологии,</p><p>634012, Томск, ул. Киевская, 111а</p></bio><bio xml:lang="en"><p>Cand. Sci. (Med.), Research Scientist, Laboratory of Experimental Cardiology,</p><p>111a, Kievskaya str., Tomsk, 634012</p></bio><email xlink:type="simple">goddess27@mail.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Научно-исследовательский институт кардиологии, Томский национальный исследовательский медицинский центр Российской академии наук</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Cardiology Research Institute, Tomsk National Research Medical Center, Russian Academy of Sciences</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2020</year></pub-date><pub-date pub-type="epub"><day>10</day><month>07</month><year>2020</year></pub-date><volume>35</volume><issue>2</issue><fpage>163</fpage><lpage>166</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Курбатов Б.К., Прокудина Е.С., 2020</copyright-statement><copyright-year>2020</copyright-year><copyright-holder xml:lang="ru">Курбатов Б.К., Прокудина Е.С.</copyright-holder><copyright-holder xml:lang="en">Kurbatov B.K., Prokudina E.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.sibjcem.ru/jour/article/view/991">https://www.sibjcem.ru/jour/article/view/991</self-uri><abstract><sec><title>Актуальность</title><p>Актуальность. На данный момент неясен патофизиологический механизм реализации повреждения сердца при синдроме такотсубо. Остается неясна роль отдельных субтипов адренорецепторов (АР) в реализации стресс-индуцированного повреждения сердца (СИПС).</p></sec><sec><title>Цель</title><p>Цель: оценить роль β-АР в реализации СИПС. Материал и методы. Исследование было выполнено на 84 крысах-самках линии Вистар. Для моделирования СИПС крысы подвергались 24-часовой иммобилизации в положении на спине. Для определения степени повреждения сердца использовали радиофармпрепарат 99mTc-пирофосфат.</p></sec><sec><title>Результаты</title><p>Результаты. Установлено, что блокада β-АР (-)-пропранололом уменьшает степень повреждения сердца на 38,4%. Показано, что селективные блокаторы β1 -АР атенолол и небиволол уменьшают степень аккумуляции 99mTc-пирофосфата в сердце в 2 и 2,55 раза соответственно. Блокада β2 -АР селективным блокатором ICI-118,551 вызывает повышение степени аккумуляции 99mTc-пирофосфата в сердце на 34,6%. Селективный блокатор β3 -АР L-748337 не оказывает эффекта на аккумуляцию 99mTc-пирофосфата в сердце.</p></sec><sec><title>Выводы</title><p>Выводы. β1 -АР участвуют в повреждающем действии стресса на сердце при иммобилизации. β2 -АР обладают кардиопротекторным эффектом при иммобилизации. β3 -АР не играют существенной роли в стресс-индуцированном повреждении сердца при однократном действии стрессора. </p></sec></abstract><trans-abstract xml:lang="en"><sec><title>Introduction</title><p>Introduction. The pathophysiological mechanisms of cardiac injury in Takotsubo syndrome are currently poorly understood. The role of adrenergic receptor (AR) subtypes in the development of stress-induced myocardial injury (SIMI) remains unclear.</p></sec><sec><title>Aim</title><p>Aim. To assess the role of β-ARs in the development of SIMI.</p></sec><sec><title>Material and Methods</title><p>Material and Methods. The study was performed using female Wistar rats (n = 84). Rats were subject to 24-hour immobilization in the supine position to simulate SIMI. 99mTc-pyrophosphate radiopharmaceutical was used to determine the degree of cardiac injury.</p></sec><sec><title>Results</title><p>Results. The study showed that β-AR blockade with propranolol reduced the degree of cardiac injury by 38.4%. Selective β1- AR antagonists, atenolol and nebivolol, led to 2.00- and 2.55-fold decreases in 99mTc pyrophosphate accumulation in the heart, respectively. Blockade of β2-ARs by a selective antagonist ICI-118.551 caused an increase in the degree of 99mTc-pyrophosphate accumulation in the heart by 34.6%. A selective β3-AR antagonist L-748337 did not affect 99mTc pyrophosphate accumulation in the heart.</p></sec><sec><title>Conclusions</title><p>Conclusions. The study showed that β1-ARs are involved in the damaging effects of stress on the heart during immobilization stress. β2-AR had a cardioprotective effect in immobilization. β3-AP did not play a significant role in the stress-induced cardiac injury with a single exposure to the stressor. </p></sec></trans-abstract><kwd-group xml:lang="ru"><kwd>синдром такотсубо</kwd><kwd>стресс-индуцированное повреждение сердца</kwd><kwd>иммобилизационный стресс</kwd><kwd>β-адренорецепторы</kwd></kwd-group><kwd-group xml:lang="en"><kwd>Takotsubo syndrome</kwd><kwd>stress-induced cardiac injury</kwd><kwd>immobilization stress</kwd><kwd>β-adrenergic receptors</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">Moritz A.R., Zamcheck N. Sudden and unexpected deaths of young soldiers; diseases responsible for such deaths during World War II. Arch. Pathol. 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