<?xml version="1.0" encoding="UTF-8"?>
<!DOCTYPE article PUBLIC "-//NLM//DTD JATS (Z39.96) Journal Publishing DTD v1.3 20210610//EN" "JATS-journalpublishing1-3.dtd">
<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">vestim</journal-id><journal-title-group><journal-title xml:lang="ru">Известия Национальной  академии наук Беларуси. Серия медицинских наук</journal-title><trans-title-group xml:lang="en"><trans-title>Proceedings of the National Academy of Sciences of Belarus, Medical series</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">1814-6023</issn><issn pub-type="epub">2524-2350</issn><publisher><publisher-name>The Republican Unitary Enterprise Publishing House "Belaruskaya Navuka"</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.29235/1814-6023-2022-19-1-38-47</article-id><article-id custom-type="elpub" pub-id-type="custom">vestim-820</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>КЛИНИЧЕСКАЯ И ЭКСПЕРИМЕНТАЛЬНАЯ МЕДИЦИНА</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>CLINICAL AND EXPERIMENTAL MEDICINE</subject></subj-group></article-categories><title-group><article-title>Эффективность дистантного ишемического посткондиционирования миокарда у крыс с индуцированным метаболическим синдромом зависит от уровня лептина</article-title><trans-title-group xml:lang="en"><trans-title>The efficiency of remote ischemic postconditioning of the myocardium in rats with induced metabolic syndrome depends on the leptin level</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>Нарыжная</surname><given-names>Н. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Naryzhnaya</surname><given-names>N. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Нарыжная Наталья Владимировна - доктор медицинских наук, ведущий научный сотрудник.</p><p>ул. Киевская, 111А, 634012, Томск.</p></bio><bio xml:lang="en"><p>Natalia V. Naryzhnaya - D. Sc. (Med.), Leading Researcher, Cardiology Research Institute of Tomsk National Research Medical Center of the Russian Academy of Sciences.</p><p>111А, Kievskaya Str., 634012, Tomsk.</p></bio><email xlink:type="simple">natalynar@yandex.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>Логвинов</surname><given-names>С. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Logvinov</surname><given-names>S. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Логвинов Сергей Валентинович - доктор медицинских наук, профессор, заведующий кафедрой, НИИ кардиологии Томского НИМЦ РАН; СибГМУ.</p><p>ул. Киевская, 111А, 634012, Томск; Московский тракт, 2, 634050, Томск.</p></bio><bio xml:lang="en"><p>Sergey V. Logvinov - D. Sc. (Med.), Professor, Head of the Department, Cardiology Research Institute of Tomsk National Research Medical Center of the Russian Academy of Sciences; Siberian State Medical University.</p><p>111А, Kievskaya Str., 634012, Tomsk; 2, Moskovski trakt, 634050, Tomsk.</p></bio><email xlink:type="simple">s_logvinov@mail.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>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>Курбатов Борис Константинович - младший научный сотрудник.</p><p>ул. Киевская, 111А, 634012, Томск.</p></bio><bio xml:lang="en"><p>Boris K. Kurbatov - Junior Researcher, Cardiology Research Institute of Tomsk National Research Medical Center of the Russian Academy of Sciences.</p><p>111А, Kievskaya Str., 634012, Tomsk.</p></bio><email xlink:type="simple">bobersanker@gmail.com</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>Мухомедзянов</surname><given-names>А. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Mukhomedzyanov</surname><given-names>A. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Мухомедзянов Александр Валерьевич - кандидат медицинских наук, младший научный сотрудник.</p><p>ул. Киевская, 111А, 634012, Томск.</p></bio><bio xml:lang="en"><p>Alexandr V. Mukhomedzyanov - Ph. D. (Med.), Junior Researcher, Cardiology Research Institute of Tomsk National Research Medical Center of the Russian Academy of Sciences.</p><p>111А, Kievskaya Str., 634012, Tomsk.</p></bio><email xlink:type="simple">sasha_m91@mail.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>Сиротина</surname><given-names>М. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Sirotina</surname><given-names>M. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Сиротина Мария Александровна - аспирант.</p><p>ул. Киевская, 111А, 634012, Томск.</p></bio><bio xml:lang="en"><p>Maria A. Sirotina - Postgraduate student, Cardiology Research Institute of Tomsk National Research Medical Center of the Russian Academy of Sciences.</p><p>111А, Kievskaya Str., 634012, Tomsk.</p></bio><email xlink:type="simple">sirotina_maria@mail.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>Чепелев</surname><given-names>С. Н.</given-names></name><name name-style="western" xml:lang="en"><surname>Chepelev</surname><given-names>S. N.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Чепелев Сергей Николаевич - старший преподаватель.</p><p>пр. Дзержинского, 83, 220116, Минск.</p></bio><bio xml:lang="en"><p>Sergey N. Chepelev - Senior Lecturer, Belarusian State Medical University.</p><p>83, Dzerzhinski Ave., 220116, Minsk.</p></bio><email xlink:type="simple">drserge1991@gmail.com</email><xref ref-type="aff" rid="aff-3"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Висмонт</surname><given-names>Ф. И.</given-names></name><name name-style="western" xml:lang="en"><surname>Vismont</surname><given-names>F. I.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Висмонт Франтишек Иванович - член-корреспондент, доктор медицинских наук, профессор, заведующий кафедрой.</p><p>пр. Дзержинского, 83, 220116, Минск.</p></bio><bio xml:lang="en"><p>Frantishek I. Vismont - Corresponding Member, D. Sc. (Med.), Professor, Head of the Department, Belarusian State Medical University.</p><p>83, Dzerzhinski Ave., 220116, Minsk.</p></bio><email xlink:type="simple">patfiz@bsmu.by</email><xref ref-type="aff" rid="aff-3"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Маслов</surname><given-names>Л. Н.</given-names></name><name name-style="western" xml:lang="en"><surname>Maslov</surname><given-names>L. N.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Маслов Леонид Николаевич - доктор медицинских наук, профессор, руководитель лаборатории.</p><p>ул. Киевская, 111А, 634012, Томск.</p></bio><bio xml:lang="en"><p>Leonid N. Maslov - D. Sc. (Med.), Professor, Head of the Laboratory, Cardiology Research Institute of Tomsk National Research Medical Center of the Russian Academy of Sciences.</p><p>111А, Kievskaya Str., 634012, Tomsk.</p></bio><email xlink:type="simple">maslov@cardio-tomsk.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 Томского национального исследовательского медицинского центра РАН</institution></aff><aff xml:lang="en"><institution>Cardiology Research Institute of Tomsk National Research Medical Center of the Russian Academy of Sciences</institution></aff></aff-alternatives><aff-alternatives id="aff-2"><aff xml:lang="ru"><institution>Научно-исследовательский институт кардиологии Томского национального исследовательского медицинского центра РАН; Сибирский государственный медицинский университет</institution></aff><aff xml:lang="en"><institution>Cardiology Research Institute of Tomsk National Research Medical Center of the Russian Academy of Sciences; Siberian State Medical University</institution></aff></aff-alternatives><aff-alternatives id="aff-3"><aff xml:lang="ru"><institution>Белорусский государственный медицинский университет</institution></aff><aff xml:lang="en"><institution>Belarusian State Medical University</institution></aff></aff-alternatives><pub-date pub-type="collection"><year>2022</year></pub-date><pub-date pub-type="epub"><day>10</day><month>03</month><year>2022</year></pub-date><volume>19</volume><issue>1</issue><fpage>38</fpage><lpage>47</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Нарыжная Н.В., Логвинов С.В., Курбатов Б.К., Мухомедзянов А.В., Сиротина М.А., Чепелев С.Н., Висмонт Ф.И., Маслов Л.Н., 2022</copyright-statement><copyright-year>2022</copyright-year><copyright-holder xml:lang="ru">Нарыжная Н.В., Логвинов С.В., Курбатов Б.К., Мухомедзянов А.В., Сиротина М.А., Чепелев С.Н., Висмонт Ф.И., Маслов Л.Н.</copyright-holder><copyright-holder xml:lang="en">Naryzhnaya N.V., Logvinov S.V., Kurbatov B.K., Mukhomedzyanov A.V., Sirotina M.A., Chepelev S.N., Vismont F.I., Maslov L.N.</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://vestimed.belnauka.by/jour/article/view/820">https://vestimed.belnauka.by/jour/article/view/820</self-uri><abstract><p>Дистантное посткондиционирование (ДПост) имеет большой терапевтический потенциал в плане защиты миокарда при ишемии-реперфузии. При этом при наличии у пациента метаболических нарушений клиническое применение кондиционирующих воздействий ограничено.</p><p>Цель настоящей работы - оценить влияние индуцированного метаболического синдрома (иМетС) на инфаркт-лимитирующий эффект дистантного ишемического посткондиционирования у крыс и изучить механизмы этого влияния. Исследование проведено на крысах линии Вистар. Для индуцирования метаболического синдрома (МетС) крыс содержали на высокоуглеводной высокожировой диете. Критериями развития МетС считали увеличение массы животного, объема абдоминального жира, развитие артериальной гипертензии, гиперхолестеринемии, гиперлептинемии, гипергликемии, повышение содержания триглицеридов в сыворотке крови, развитие состояния инсулинорезистентности по значимому повышению индекса Homeostatic Model Assessment of Insulin Resistance (HOMA-IR) и нарушение толерантности к глюкозе. Всем животным моделировали 45-минутную коронароокклюзию и 120-минутную реперфузию.</p><p>ДПост приводило к двукратному сокращению размера инфаркта у крыс с интактным метаболизмом (р &lt; 0,0001), в то время как у крыс с иМетС уменьшение размера инфаркта при ДПост составило 25 % (р = 0,00003), что было значимо ниже, чем у животных без иМетС (р &lt; 0,0001). Выявлена прямая корреляционная зависимость размера инфаркта при ДПост от содержания лептина в сыворотке крови крыс с иМетС.</p><p>Анализ полученных данных позволяет сделать предположение о том, что снижение эффективности ДПост у крыс с индуцированным диетой МетС зависит от содержания лептина в крови.</p></abstract><trans-abstract xml:lang="en"><p>Remote postconditioning (RPost) has a great therapeutic potential for protecting the myocardium during ischemiareperfusion in clinical practice. At the same time, an important problem limiting the use of conditioning effects in the clinic is the presence of metabolic disorders in the patient. The aim of this work was to assess the effect of induced metabolic syndrome (iMetS) on the efficacy of the infarct-limiting effect of remote ischemic postconditioning (RPost) in rats and to study the mechanisms of this effect.</p><p>The study was carried out on Wistar rats. MetS was induced by high-carbohydrate high-fat diet. Criteria of metabolic syndrome were an increase in the weight of animals, abdominal fat volume, the development of arterial hypertension, hypercholesterolemia, an increase in triglycerides in serum, hyperleptinemia, hyperglycemia, the development of a state of insulin resistance by a significant increase in the Homeostatic Model Assessment of Insulin Resistance (HOMA-IR) index and glucose tolerance. All animals were subjected to 45 min coronary occlusion and 120 min reperfusion.</p><p>RPost led to a twofold reduction of infarct size in rats with intact metabolism (р &lt; 0.0001), while in rats with iMetS a decrease in infarct size during RPost was 25 % (p = 0.00003), which was significantly lower than in animals without iMetC (р &lt; 0.0001). A direct correlation was found between of infarct size during RPost and the serum leptin level of rats with iMetC.</p><p>The presented data suggested that a decrease in the efficiency of remote postconditioning in rats with diet-induced metabolic syndrome depends on leptin content in blood.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>дистантное посткондиционирование</kwd><kwd>метаболический синдром</kwd><kwd>миокард</kwd><kwd>ишемия</kwd><kwd>реперфузия</kwd><kwd>артериальное давление</kwd><kwd>лептин</kwd><kwd>глюкоза</kwd><kwd>триглицериды</kwd><kwd>инсулин</kwd></kwd-group><kwd-group xml:lang="en"><kwd>distant postconditioning</kwd><kwd>metabolic syndrome</kwd><kwd>myocardium</kwd><kwd>ischemia</kwd><kwd>reperfusion</kwd><kwd>arterial pessure</kwd><kwd>leptin</kwd><kwd>glucose</kwd><kwd>triacyl glyceride</kwd><kwd>insulin</kwd></kwd-group><funding-group><funding-statement xml:lang="ru">Работа выполнена при поддержке Российского научного фонда (грант 22-45-02005). Исследования с лептином проводились в рамках государственного задания АААА-А15-115120910024-0.</funding-statement><funding-statement xml:lang="en">This study was supported by the Russian Science Foundation (grant 22-45-02005). The leptin studies were carried out within the framework of the state assignments AAAA-A15-115120910024-0.</funding-statement></funding-group></article-meta></front><back><ref-list><title>References</title><ref id="cit1"><label>1</label><citation-alternatives><mixed-citation xml:lang="ru">Braunwald, E. The war against heart failure: the Lancet lecture / E. Braunwald // Lancet. - 2015. - Vol. 385, N 9970. -P. 812-824. https://doi.org/10.1016/S0140-6736(14)61889-4</mixed-citation><mixed-citation xml:lang="en">Braunwald E. The war against heart failure: the Lancet lecture. Lancet, 2015, vol. 385, no. 9970, pp. 812-824. https://doi.org/10.1016/S0140-6736(14)61889-4</mixed-citation></citation-alternatives></ref><ref id="cit2"><label>2</label><citation-alternatives><mixed-citation xml:lang="ru">The mitochondrial permeability transition pore and its role in myocardial ischemia reperfusion injury / S. B. Ong [et al.] // J. Mol. Cell. Cardiol. - 2015. - Vol. 78. - P. 23-34. https://doi.org/10.1016/j.yjmcc.2014.11.005</mixed-citation><mixed-citation xml:lang="en">Ong S. B., Samangouei P., Kalkhoran S. B., Hausenloy D. J. The mitochondrial permeability transition pore and its role in myocardial ischemia reperfusion injury. Journal of Molecular and Cellular Cardiology, 2015, vol. 78, pp. 23-34. https://doi.org/10.1016/j.yjmcc.2014.11.005</mixed-citation></citation-alternatives></ref><ref id="cit3"><label>3</label><citation-alternatives><mixed-citation xml:lang="ru">Effect of hyperglycaemia and diabetes on acute myocardial ischaemia-reperfusion injury and cardioprotection by ischaemic conditioning protocols / C. Penna [et al.] // Br. J. Pharmacol. - 2020. - Vol. 177, N 23. - P. 5312-5335. https://doi.org/10.1111/bph.14993</mixed-citation><mixed-citation xml:lang="en">Penna C., Andreadou I., Aragno M., Beauloye C., Bertrand L., Lazou A. [et al.]. Effect of hyperglycaemia and diabetes on acute myocardial ischaemia-reperfusion injury and cardioprotection by ischaemic conditioning protocols. British Journal of Pharmacology, 2020, vol. 177, no. 23, pp. 5312-5335. https://doi.org/10.1111/bph.14993</mixed-citation></citation-alternatives></ref><ref id="cit4"><label>4</label><citation-alternatives><mixed-citation xml:lang="ru">Remote ischaemic pre- and delayed postconditioning - similar degree of cardioprotection but distinct mechanisms / M. Basalay [et al.] // Exp. Physiol. - 2012. - Vol. 97, N 8. - P. 908-917. https://doi.org/10.1113/expphysiol.2012.064923</mixed-citation><mixed-citation xml:lang="en">Basalay M., Barsukevich V., Mastitskaya S., Mrochek A., Pernow J., Sjoquist P. O., Ackland G. L., Gourine A. V., Gourine A. Remote ischaemic pre- and delayed postconditioning - similar degree of cardioprotection but distinct mechanisms. Experimental Physiology, 2012, vol. 97, no. 8, pp. 908-917. https://doi.org/10.1113/expphysiol.2012.064923</mixed-citation></citation-alternatives></ref><ref id="cit5"><label>5</label><citation-alternatives><mixed-citation xml:lang="ru">Vinten-Johansen, J. The science and clinical translation of remote postconditioning / J. Vinten-Johansen, W. J. Shi // J. Cardiovasc. Med. - 2013. - Vol. 14, N 3. - P. 206-213. https://doi.org/10.2459/JCM.0b013e32835cecc6</mixed-citation><mixed-citation xml:lang="en">Vinten-Johansen J., Shi W. The science and clinical translation of remote postconditioning. Journal of Cardiovascular Medicine (Hagerstown), 2013, vol. 14, no. 3, pp. 206-213. https://doi.org/10.2459/JCM.0b013e32835cecc6</mixed-citation></citation-alternatives></ref><ref id="cit6"><label>6</label><citation-alternatives><mixed-citation xml:lang="ru">Inhibition of myocardial injury by ischemic postconditioning during reperfusion: comparison with ischemic preconditioning / Z. Q. Zhao [et al.] // Am. J. Physiol. Circ. Physiol. - 2003. - Vol. 285, N 2. - P. H579-H588. https://doi.org/10.1152/ajpheart.01064.2002</mixed-citation><mixed-citation xml:lang="en">Zhao Z. Q., Corvera J. S., Halkos M. E., Kerendi F., Wang N. P., Guyton R. A., Vinten-Johansen J. Inhibition of myocardial injury by ischemic postconditioning during reperfusion: comparison with ischemic preconditioning. American Journal of Physiology Heart and Circulatory Physiology, 2003, vol. 285, no. 2, pp. H579-H588. https://doi.org/10.1152/ajpheart.01064.2002</mixed-citation></citation-alternatives></ref><ref id="cit7"><label>7</label><citation-alternatives><mixed-citation xml:lang="ru">Molecular mechanisms of obesity-linked cardiac dysfunction: an up-date on current knowledge / J. Gutierrez-Cuevas [et al.] // Cells. - 2021. - Vol. 10, N 3. - P. 629. https://doi.org/10.3390/cells10030629</mixed-citation><mixed-citation xml:lang="en">Gutierrez-Cuevas J., Sandoval-Rodriguez A., Meza-Rios A., Monroy-Ramnez H. C., Galicia-Moreno M., Garda-Banuelos J., Santos A., Armendariz-Borunda J. Molecular mechanisms of obesity-linked cardiac dysfunction: an up-date on current knowledge. Cells, 2021, vol. 10, no. 3, p. 629. https://doi.org/10.3390/cells10030629</mixed-citation></citation-alternatives></ref><ref id="cit8"><label>8</label><citation-alternatives><mixed-citation xml:lang="ru">Postconditioning fails to reduce the infarct sizes in hearts from rats with metabolic syndrome: role of glycogen synthase kinase 3beta / C. ReuBner [et al.] // J. Mol. Cell. Cardiol. - 2006. - Vol. 40, N 6. - Art. 970. https://doi.org/10.1016/j.yjmcc.2006.03.150</mixed-citation><mixed-citation xml:lang="en">ReuBner C., Kloting I., Strasser R. H., Weinbrenner C. Postconditioning fails to reduce the infarct sizes in hearts from rats with metabolic syndrome: role of glycogen synthase kinase 3beta. Journal of Molecular and Cellular Cardiology, 2006, vol. 40, no. 6, art. 970. https://doi.org/10.1016/j.yjmcc.2006.03.150</mixed-citation></citation-alternatives></ref><ref id="cit9"><label>9</label><citation-alternatives><mixed-citation xml:lang="ru">Autophagy is involved in the cardioprotection effect of remote limb ischemic postconditioning on myocardial ischemia/ reperfusion injury in normal mice, but not diabetic mice / Z. Han [et al.] // PLoS ONE. - 2014. - Vol. 9, N 1. - P. e86838. https://doi.org/10.1371/journal.pone.0086838</mixed-citation><mixed-citation xml:lang="en">Han Z., Cao J., Song D., Tian L., Chen K., Wang Y., Gao L., Yin Z., Fan Y., Wang C. Autophagy is involved in the cardioprotection effect of remote limb ischemic postconditioning on myocardial ischemia/reperfusion injury in normal mice, but not diabetic mice. PLoS ONE, 2014, vol. 9, no. 1, p. e86838. https://doi.org/10.1371/journal.pone.0086838</mixed-citation></citation-alternatives></ref><ref id="cit10"><label>10</label><citation-alternatives><mixed-citation xml:lang="ru">Hyperlipidaemia and cardioprotection: Animal models for translational studies / I. Andreadou [et al.] // Br. J. Pharmacol. -2020. - Vol. 177, N 23. - P. 5287-5311. https://doi.org/10.1111/bph.14931</mixed-citation><mixed-citation xml:lang="en">Andreadou I., Schulz R., Badimon L., Adameova A., Kleinbongard P., Lecour S. [et al.]. Hyperlipidaemia and cardioprotection: animal models for translational studies. British Journal of Pharmacology, 2020, vol. 177, no. 23, pp. 5287-5311. https://doi.org/10.1111/bph.14931</mixed-citation></citation-alternatives></ref><ref id="cit11"><label>11</label><citation-alternatives><mixed-citation xml:lang="ru">Acute hyperglycemia abolishes cardioprotection by remote ischemic perconditioning / T. Baranyai [et al.] // Cardiovasc. Diabet. - 2015. - Vol. 14. - Art. 151. https://doi.org/10.1186/s12933-015-0313-1</mixed-citation><mixed-citation xml:lang="en">Baranyai T., Nagy C. T., Koncsos G., Onodi Z., Karolyi-Szabo M., Makkos A., Varga Z. V., Ferdinandy P., Giricz Z. Acute hyperglycemia abolishes cardioprotection by remote ischemic perconditioning. Cardiovascular Diabetology, 2015, vol. 14, art. 151. https://doi.org/10.1186/s12933-015-0313-1</mixed-citation></citation-alternatives></ref><ref id="cit12"><label>12</label><citation-alternatives><mixed-citation xml:lang="ru">Long-term effect of remote ischemic conditioning on infarct size and clinical outcomes in patients with anterior ST-elevation myocardial infarction / D. Verouhis [et al.] // Catheter. Cardiovasc. Interv. - 2021. - Vol. 97, N 3. - P. 386-392. https://doi.org/10.1002/ccd.28760</mixed-citation><mixed-citation xml:lang="en">Verouhis D., Sorensson P., Gourine A., Henareh L., Persson J., Saleh N. [et al.]. Long-term effect of remote ischemic conditioning on infarct size and clinical outcomes in patients with anterior ST-elevation myocardial infarction. Catheterization and Cardiovascular Interventions, 2021, vol. 97, no. 3, pp. 386-392. https://doi.org/10.1002/ccd.28760</mixed-citation></citation-alternatives></ref><ref id="cit13"><label>13</label><citation-alternatives><mixed-citation xml:lang="ru">Diabetes mellitus and the metabolic syndrome do not abolish, but might reduce, the cardioprotective effect of ischemic postconditioning / W. Oosterlinck [et al.] // J. Thorac. Cardiovasc. Surg. - 2013. - Vol. 145, N 6. - P. 1595-1602. https://doi.org/10.1016/j.jtcvs.2013.02.016</mixed-citation><mixed-citation xml:lang="en">Oosterlinck W., Dresselaers T., Geldhof V., Nevelsteen I., Janssens S., Himmelreich U., Herijgers P. Diabetes mellitus and the metabolic syndrome do not abolish, but might reduce, the cardioprotective effect of ischemic postconditioning. Journal of Thoracic and Cardiovascular Surgery, 2013, vol. 145, no. 6, pp. 1595-1602. https://doi.org/10.1016/j.jtcvs.2013.02.016</mixed-citation></citation-alternatives></ref><ref id="cit14"><label>14</label><citation-alternatives><mixed-citation xml:lang="ru">High carbohydrate high fat diet induces the production of connective tissue growth factors, increased blood pressure, and changes in the aortic wall in aged rats / N. Naryzhnaya [et al.] // FASEB J. - 2021. - Vol. 35, N S1. https://doi.org/10.1096/fasebj.2021.35.S1.05125</mixed-citation><mixed-citation xml:lang="en">Naryzhnaya N., Kurbatov B., Gorbunov A., Derkachev I., Logvinov S., Birulina J., Maslov L. High carbohydrate high fat diet induces the production of connective tissue growth factors, increased blood pressure, and changes in the aortic wall in aged rats. FASEB Journal, 2021, vol. 35, no. S1. https://doi.org/10.1096/fasebj.2021.35.S1.05125</mixed-citation></citation-alternatives></ref><ref id="cit15"><label>15</label><citation-alternatives><mixed-citation xml:lang="ru">Cardioprotective effect of chronic hypoxia is blunted by concomitant hypercapnia / J. Neckar [et al.] // Physiol. Res. -2003. - Vol. 52, N 2. - P. 171-175.</mixed-citation><mixed-citation xml:lang="en">Neckar J., Szarszoi O., Herget J., Ostadal B., Kolar F. Cardioprotective effect of chronic hypoxia is blunted by concomitant hypercapnia. Physiological Research, 2003, vol. 52, no. 2, pp. 171-175.</mixed-citation></citation-alternatives></ref><ref id="cit16"><label>16</label><citation-alternatives><mixed-citation xml:lang="ru">Global, regional, and national comparative risk assessment of 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks, 1990-201 5: a systematic analysis for the Global Burden of Disease Study 2015 / M. N. Forouzanfar [et al.] // Lancet. - 2016. - Vol. 388, N 10053. - P. 1659-724. https://doi.org/10.1016/S0140-6736(16)31679-8</mixed-citation><mixed-citation xml:lang="en">GBD 2015 Risk Factors Collaborators. Global, regional, and national comparative risk assessment of 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks, 1990-2015: a systematic analysis for the Global Burden of Disease Study 2015. Lancet, 2016, vol. 388, no. 10053, pp. 1659-724. https://doi.org/10.1016/S0140-6736(16)31679-8</mixed-citation></citation-alternatives></ref><ref id="cit17"><label>17</label><citation-alternatives><mixed-citation xml:lang="ru">Acute hyperglycaemia enhances oxidative stress and aggravates myocardial ischaemia/reperfusion injury: role of thioredoxin-interacting protein / H. Su [et al.] // J. Cell. Mol. Med. - 2013. - Vol. 17, N 1. - P. 181-191. https://doi.org/10.1111/j.1582-4934.2012.01661.x</mixed-citation><mixed-citation xml:lang="en">Su H., Ji L., Xing W., Zhang W., Zhou H., Qian X., Wang X., Gao F., Sun X., Zhang H. Acute hyperglycaemia enhances oxidative stress and aggravates myocardial ischaemia/reperfusion injury: role of thioredoxin-interacting protein. Journal of Cellular and Molecular Medicine, 2013, vol. 17, no. 1, pp. 181-191. https://doi.org/10.1111/j.1582-4934.2012.01661.x</mixed-citation></citation-alternatives></ref><ref id="cit18"><label>18</label><citation-alternatives><mixed-citation xml:lang="ru">Long-chain free fatty acids inhibit ischaemic preconditioning of the isolated rat heart / A. Lochner [et al.] // Mol. Cell. Biochem. - 2020. - Vol. 473, N 1-2. - P. 111-132. https://doi.org/10.1007/s11010-020-03812-9</mixed-citation><mixed-citation xml:lang="en">Lochner A., Genade S., Genis A., Marais E., Salie R. Long-chain free fatty acids inhibit ischaemic preconditioning of the isolated rat heart. Molecular and Cellular Biochemistry, 2020, vol. 473, no. 1-2, pp. 111-132. https://doi.org/10.1007/s11010-020-03812-9</mixed-citation></citation-alternatives></ref><ref id="cit19"><label>19</label><citation-alternatives><mixed-citation xml:lang="ru">Myocardial susceptibility to ischaemia/reperfusion in obesity: a re-evaluation of the effects of age / I. Webster [et al.] // BMC Physiol. - 2017. - Vol. 17, N 1. - Art. 3. https://doi.org/10.1186/s12899-017-0030-y</mixed-citation><mixed-citation xml:lang="en">Webster I., Salie R., Marais E., Fan W. J., Maarman G., Huisamen B., Lochner A. Myocardial susceptibility to ischaemia/ reperfusion in obesity: a re-evaluation of the effects of age. BMC Physiology, 2017, vol. 17, no. 1, art. 3. https://doi.org/10.1186/s12899-017-0030-y</mixed-citation></citation-alternatives></ref><ref id="cit20"><label>20</label><citation-alternatives><mixed-citation xml:lang="ru">Ischaemic preconditioning does not protect the heart in obese and lean animal models of type 2 diabetes / S. B. Kristiansen [et al.] // Diabetologia. - 2004. - Vol. 47, N 10. - P. 1716-1721. https://doi.org/10.1007/s00125-004-1514-4</mixed-citation><mixed-citation xml:lang="en">Kristiansen S. B., L0fgren B., St0ttrup N. B., Khatir D., Nielsen-Kudsk J. E., Nielsen T. T., B0tker H. E., Flyvbjerg A. Ischaemic preconditioning does not protect the heart in obese and lean animal models of type 2 diabetes. Diabetologia, 2004, vol. 47, no. 10, pp. 1716-1721. https://doi.org/10.1007/s00125-004-1514-4</mixed-citation></citation-alternatives></ref><ref id="cit21"><label>21</label><citation-alternatives><mixed-citation xml:lang="ru">Zhu, S. G. Type 2 diabetic obese db/db mice are refractory to myocardial ischaemic post-conditioning in vivo: potential role for Hsp20, F1-ATPase 5 and Echs1 / S. G. Zhu, L. Xi, R. C. Kukreja // J. Cell. Mol. Med. - 2012. - Vol. 16, N 4. -P. 950-958. https://doi.org/10.1111/j.1582-4934.2011.01376.x</mixed-citation><mixed-citation xml:lang="en">Zhu S. G., Xi L., Kukreja R. C. Type 2 diabetic obese db/db mice are refractory to myocardial ischaemic post-conditioning in vivo: potential role for Hsp20, F1-ATPase 5 and Echs1. Journal of Cellular and Molecular Medicine, 2012, vol. 16, no. 4, pp. 950-958. https://doi.org/10.1111/j.1582-4934.2011.01376.x</mixed-citation></citation-alternatives></ref><ref id="cit22"><label>22</label><citation-alternatives><mixed-citation xml:lang="ru">Angiotensin-converting enzyme inhibition and food restriction restore delayed preconditioning in diabetic mice / G. van der Mieren [et al.] // Cardiovasc. Diabetol. - 2013. - Vol. 12, N 1. - P. 36. https://doi.org/10.1186/1475-2840-12-36</mixed-citation><mixed-citation xml:lang="en">van der Mieren G., Nevelsteen I., Vanderper A., Oosterlinck W., Flameng W., Herijgers P. Angiotensin-converting enzyme inhibition and food restriction restore delayed preconditioning in diabetic mice. Cardiovascular Diabetology, 2013, vol. 12, no. 1, p. 36. https://doi.org/10.1186/1475-2840-12-36</mixed-citation></citation-alternatives></ref><ref id="cit23"><label>23</label><citation-alternatives><mixed-citation xml:lang="ru">Hypertrophic adipocyte-derived exosomal mir-802-5p contributes to insulin resistance in cardiac myocytes through targeting HSP60 / Z. Wen [et al.] // Obesity. - 2020. - Vol. 28, N 10. - P. 1932-1940. https://doi.org/10.1002/oby.22932</mixed-citation><mixed-citation xml:lang="en">Wen Z., Li J., Fu Y., Zheng Y., Ma M., Wang C. Hypertrophic adipocyte-derived exosomal miR-802-5p contributes to insulin resistance in cardiac myocytes through targeting HSP60. Obesity, 2020, vol. 28, no. 10, pp. 1932-1940. https://doi.org/10.1002/oby.22932</mixed-citation></citation-alternatives></ref><ref id="cit24"><label>24</label><citation-alternatives><mixed-citation xml:lang="ru">Adipokines: new potential therapeutic target for obesity and metabolic, rheumatic, and cardiovascular diseases / L. Recinella [et al.] // Front Physiol. - 2020. - Vol. 11. - P. 578966. https://doi.org/10.3389/fphys.2020.578966/full</mixed-citation><mixed-citation xml:lang="en">Recinella L., Orlando G., Ferrante C., Chiavaroli A., Brunetti L., Leone S. Adipokines: new potential therapeutic target for obesity and metabolic,rheumatic, and cardiovascular diseases. Frontiers in Physiology, 2020, vol. 11, p. 578966. https://doi.org/10.3389/fphys.2020.578966/full</mixed-citation></citation-alternatives></ref><ref id="cit25"><label>25</label><citation-alternatives><mixed-citation xml:lang="ru">Chronic type 2 but not type 1 diabetes impairs myocardial ischaemic tolerance and preconditioning in C57Bl/6 mice / J. S. Russell [et al.] // Exp. Physiol. - 2019. - Vol. 104, N 12. - P. 1868-1880. https://doi.org/10.1113/EP088024</mixed-citation><mixed-citation xml:lang="en">Russell J. S., Griffith T. A., Helman T., Du Toit E. F., Peart J. N., Headrick J. P. Chronic type 2 but not type 1 diabetes impairs myocardial ischaemic tolerance and preconditioning in C57Bl/6 mice. Experimental Physiology, 2019, vol. 104, no. 12, pp. 1868-1880. https://doi.org/10.1113/EP088024</mixed-citation></citation-alternatives></ref><ref id="cit26"><label>26</label><citation-alternatives><mixed-citation xml:lang="ru">Leptin regulates MMP-2, TIMP-1 and collagen synthesis via p38 MAPK in HL-1 murine cardiomyocytes / K. Schram [et al.] // Cell. Mol. Biol. Lett. - 2010. - Vol. 15, N 4. - P. 551-563. https://doi.org/10.2478/s11658-010-0027-z/html</mixed-citation><mixed-citation xml:lang="en">Schram K., De Girolamo S., Madani S., Munoz D., Thong F., Sweeney G. Leptin regulates MMP-2, TIMP-1 and collagen synthesis via p38 MAPK in HL-1 murine cardiomyocytes. Cellular &amp; Molecular Biology Letters, 2010, vol. 15, no. 4, pp. 551-563. https://doi.org/10.2478/s11658-010-0027-z/html</mixed-citation></citation-alternatives></ref><ref id="cit27"><label>27</label><citation-alternatives><mixed-citation xml:lang="ru">Postconditioning attenuates cardiomyocyte apoptosis via inhibition of JNK and p38 mitogen-activated protein kinase signaling pathways / H. Y. Sun [et al.] // Apoptosis. - 2006. - Vol. 11, N 9. - P. 1583-1593. https://doi.org/10.1007/s10495-006-9037-8</mixed-citation><mixed-citation xml:lang="en">Sun H. Y., Wang N. P., Halkos M., Kerendi F., Kin H., Guyton R. A., Vinten-Johansen J., Zhao Z. Q. Postconditioning attenuates cardiomyocyte apoptosis via inhibition of JNK and p38 mitogen-activated protein kinase signaling pathways. Apoptosis, 2006, vol. 11, no. 9, pp. 1583-1593. https://doi.org/10.1007/s10495-006-9037-8</mixed-citation></citation-alternatives></ref><ref id="cit28"><label>28</label><citation-alternatives><mixed-citation xml:lang="ru">Leptin and obesity: role and clinical implication / M. Obradovic [et al.] // Front Endocrinol. (Lausanne). - 2021. -Vol. 12. - Art. 585887. https://doi.org/10.3389/fendo.2021.585887</mixed-citation><mixed-citation xml:lang="en">Obradovic M., Sudar-Milovanovic E., Soskic S., Essack M., Arya S., Stewart A. J., Gojobori T., Isenovic E. R. Leptin and obesity: role and clinical implication. Frontiers in Endocrinology (Lausanne), 2021, vol. 12, art. 585887. https://doi.org/10.3389/fendo.2021.585887</mixed-citation></citation-alternatives></ref><ref id="cit29"><label>29</label><citation-alternatives><mixed-citation xml:lang="ru">High-fat diet-induced obesity leads to resistance to leptin-induced cardiomyocyte contractile response / J. Ren [et al.] // Obesity. - 2008. - Vol. 16, N 11. - P. 2417-2423. https://doi.org/10.1038/oby.2008.38</mixed-citation><mixed-citation xml:lang="en">Ren J., Zhu B. H., Relling D. P., Esberg L. B., Ceylan-Isik A. F. High-fat diet-induced obesity leads to resistance to leptin-induced cardiomyocyte contractile response. Obesity, 2008, vol. 16, no. 11, pp. 2417-2423. https://doi.org/10.1038/oby.2008.38</mixed-citation></citation-alternatives></ref><ref id="cit30"><label>30</label><citation-alternatives><mixed-citation xml:lang="ru">Xu, T. Amelioration of myocardial ischemia/reperfusion injury by leptin pretreatment and ischemic preconditioning in mouse / T.-T. Xu, S.-P. Liu, X.-S. Wang // Zhongguo Wei Zhong Bing Ji Jiu Yi Xue. - 2010. - Vol. 22, N 2. - P. 105-108.</mixed-citation><mixed-citation xml:lang="en">Xu T.-T., Liu S.-P., Wang X.-S. Wang Amelioration of myocardial ischemia/reperfusion injury by leptin pretreatment and ischemic preconditioning in mouse. Zhongguo Wei Zhong Bing Ji Jiu Yi Xue, 2010, vol. 22, no. 2, pp. 105-108.</mixed-citation></citation-alternatives></ref></ref-list><fn-group><fn fn-type="conflict"><p>The authors declare that there are no conflicts of interest present.</p></fn></fn-group></back></article>
