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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">cardiovascular</journal-id><journal-title-group><journal-title xml:lang="ru">Кардиоваскулярная терапия и профилактика</journal-title><trans-title-group xml:lang="en"><trans-title>Cardiovascular Therapy and Prevention</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">1728-8800</issn><issn pub-type="epub">2619-0125</issn><publisher><publisher-name>«SILICEA-POLIGRAF» LLC</publisher-name></publisher></journal-meta><article-meta><article-id custom-type="elpub" pub-id-type="custom">cardiovascular-2184</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>МНЕНИЕ ПО ПРОБЛЕМЕ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>OPINION ON A PROBLEM</subject></subj-group></article-categories><title-group><article-title>Механизмы повреждения миокарда при операциях коронарного шунтирования</article-title><trans-title-group xml:lang="en"><trans-title>Myocardial damage mechanisms in coronary artery bypass surgery (literature review)</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>Самадов</surname><given-names>Ш. Х.</given-names></name><name name-style="western" xml:lang="en"><surname>Samadov</surname><given-names>Sh. Kh.</given-names></name></name-alternatives><bio xml:lang="ru"><p>аспирант клинико-диагностического отделения</p></bio><email xlink:type="simple">buziashvili@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>Кокшенева</surname><given-names>И. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Koksheneva</surname><given-names>I. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>с.н.с. клинико-диагностического отделения</p></bio><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Научный центр сердечно-сосудистой хирургии им. А.Н.Бакулева РАМН. Москва</institution></aff><aff xml:lang="en"><institution>A.N. Bakoulev Research Centre for Cardiovascular Surgery, Russian Academy of Medical Sciences. Moscow</institution></aff></aff-alternatives><pub-date pub-type="collection"><year>2010</year></pub-date><pub-date pub-type="epub"><day>01</day><month>01</month><year>1970</year></pub-date><volume>9</volume><issue>8</issue><fpage>75</fpage><lpage>80</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Самадов Ш.Х., Кокшенева И.В., 1970</copyright-statement><copyright-year>1970</copyright-year><copyright-holder xml:lang="ru">Самадов Ш.Х., Кокшенева И.В.</copyright-holder><copyright-holder xml:lang="en">Samadov S.K., Koksheneva I.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://cardiovascular.elpub.ru/jour/article/view/2184">https://cardiovascular.elpub.ru/jour/article/view/2184</self-uri><abstract><p>Статья посвящена рассмотрению современных научных представлений о механизмах повреждения миокарда при операциях коронарного шунтирования. Представлены современные публикации по данной проблеме — молекулярная основа и патофизиологические закономерности, развивающиеся при синдроме ишемии/реперфузии, рассматриваются возможные кардиопротективные стратегии.</p></abstract><trans-abstract xml:lang="en"><p>The paper discusses modern views on myocardial damage mechanisms in coronary artery bypass surgery (CABG). The publications reviewed include those on molecular basis and pathophysiological pathways in ischemia/ reperfusion syndrome, as well as on potential cardioprotective strategies.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>аортокоронарное шунтирование</kwd><kwd>реперфузионное поврежедние миокарда</kwd><kwd>миокардиальный станнинг</kwd><kwd>воспалительный ответ</kwd><kwd>антиишемическпе стратегии</kwd><kwd>кардиопротекция</kwd></kwd-group><kwd-group xml:lang="en"><kwd>coronary artery bypass surgery</kwd><kwd>reperfusion myocardial damage</kwd><kwd>myocardial stunning</kwd><kwd>inflammatory response</kwd><kwd>anti-ischemic strategies</kwd><kwd>cardioprotection</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">Бокерия Л.А., Чичерин И.Н. Природа и клиническое значение “новых ишемических синдромов”. Москва. Изд. НЦ ССХ им.А.Н.Бакулева РАМН 2007.</mixed-citation><mixed-citation xml:lang="en">Бокерия Л.А., Чичерин И.Н. Природа и клиническое значение “новых ишемических синдромов”. Москва. Изд. НЦ ССХ им.А.Н.Бакулева РАМН 2007.</mixed-citation></citation-alternatives></ref><ref id="cit2"><label>2</label><citation-alternatives><mixed-citation xml:lang="ru">Andrukhiv A, Costa AD, West IC, et al. Opening mitoKatp increases superoxide generation from complex 1 of the electron transport chain. Am J Physiol Heart Circ Physiol 2006; 29: H2067-74.</mixed-citation><mixed-citation xml:lang="en">Andrukhiv A, Costa AD, West IC, et al. Opening mitoKatp increases superoxide generation from complex 1 of the electron transport chain. Am J Physiol Heart Circ Physiol 2006; 29: H2067-74.</mixed-citation></citation-alternatives></ref><ref id="cit3"><label>3</label><citation-alternatives><mixed-citation xml:lang="ru">Anselmi A, Abbate A, Girola F, et al. Myocardial ischemia, stunning, inflammation, and apoptosis during cardiac surgery: a review of evidence. Eur J Cardiothorac Surg 2004; 25: 304-11.</mixed-citation><mixed-citation xml:lang="en">Anselmi A, Abbate A, Girola F, et al. Myocardial ischemia, stunning, inflammation, and apoptosis during cardiac surgery: a review of evidence. Eur J Cardiothorac Surg 2004; 25: 304-11.</mixed-citation></citation-alternatives></ref><ref id="cit4"><label>4</label><citation-alternatives><mixed-citation xml:lang="ru">Baines CP, Molkentin JD. STRESS signaling pathways that modulate cardiac myocyte apoptosis. J Mol Cell Cardiol 2005; 38(1): 47-62.</mixed-citation><mixed-citation xml:lang="en">Baines CP, Molkentin JD. STRESS signaling pathways that modulate cardiac myocyte apoptosis. J Mol Cell Cardiol 2005; 38(1): 47-62.</mixed-citation></citation-alternatives></ref><ref id="cit5"><label>5</label><citation-alternatives><mixed-citation xml:lang="ru">Birdi I, Angelini GD, Bryan AJ. Biochemical markers of myocardial injury during cardiac operations. Ann Thorac Surg 1997; 63: 879-84.</mixed-citation><mixed-citation xml:lang="en">Birdi I, Angelini GD, Bryan AJ. Biochemical markers of myocardial injury during cardiac operations. Ann Thorac Surg 1997; 63: 879-84.</mixed-citation></citation-alternatives></ref><ref id="cit6"><label>6</label><citation-alternatives><mixed-citation xml:lang="ru">Canton M, Skyschally A, Menabo R, et al. Oxidative modification of tropomyosin and myocardial dysfunction following coronary microembolization. Eur Heart J 2006; 27: 875-81.</mixed-citation><mixed-citation xml:lang="en">Canton M, Skyschally A, Menabo R, et al. Oxidative modification of tropomyosin and myocardial dysfunction following coronary microembolization. Eur Heart J 2006; 27: 875-81.</mixed-citation></citation-alternatives></ref><ref id="cit7"><label>7</label><citation-alternatives><mixed-citation xml:lang="ru">Carlucci F, Tabucchi A, Biagioli B, et al. Cardiac surgery: myocardial energy balance, antioxidant status and endothelial function after ischemia- reperfusion. Biomed Pharmacother 2002; 56: 483-91.</mixed-citation><mixed-citation xml:lang="en">Carlucci F, Tabucchi A, Biagioli B, et al. Cardiac surgery: myocardial energy balance, antioxidant status and endothelial function after ischemia- reperfusion. Biomed Pharmacother 2002; 56: 483-91.</mixed-citation></citation-alternatives></ref><ref id="cit8"><label>8</label><citation-alternatives><mixed-citation xml:lang="ru">Dirksen MT, Laarman GJ, Simoons ML, et al. Reperfusion injury in humans: a review of clinical trials on reperfusion injury inhibitory strategies. Cardiovasc Res 2007: 343-55.</mixed-citation><mixed-citation xml:lang="en">Dirksen MT, Laarman GJ, Simoons ML, et al. Reperfusion injury in humans: a review of clinical trials on reperfusion injury inhibitory strategies. Cardiovasc Res 2007: 343-55.</mixed-citation></citation-alternatives></ref><ref id="cit9"><label>9</label><citation-alternatives><mixed-citation xml:lang="ru">Galinanes M, James M, Codd V, et al. TNF- gene promoter polymorphism at nucleotide-308 and the inflammatory response and oxidative stress induced by cardiac surgery: role of heart failure and medical treatment. Eur J Cardiothorac Surg 2008; 34: 332-7.</mixed-citation><mixed-citation xml:lang="en">Galinanes M, James M, Codd V, et al. TNF- gene promoter polymorphism at nucleotide-308 and the inflammatory response and oxidative stress induced by cardiac surgery: role of heart failure and medical treatment. Eur J Cardiothorac Surg 2008; 34: 332-7.</mixed-citation></citation-alternatives></ref><ref id="cit10"><label>10</label><citation-alternatives><mixed-citation xml:lang="ru">Heusch Ph, Skyschally A, Leineweber K, et al. The interaction of coronary microembolization and ischemic preconditioning: A third window of cardioprotection through THF-alpha. Arch Med Sci 2007; 2: 83-92.</mixed-citation><mixed-citation xml:lang="en">Heusch Ph, Skyschally A, Leineweber K, et al. The interaction of coronary microembolization and ischemic preconditioning: A third window of cardioprotection through THF-alpha. Arch Med Sci 2007; 2: 83-92.</mixed-citation></citation-alternatives></ref><ref id="cit11"><label>11</label><citation-alternatives><mixed-citation xml:lang="ru">Joashi U, Tibby SM, Turner C, et al. Soluble Fas may be a proinflammatory marker after cardiopulmonary bypass in children. J Thorac Cardiovasc Surg 2002; 123: 137-44.</mixed-citation><mixed-citation xml:lang="en">Joashi U, Tibby SM, Turner C, et al. Soluble Fas may be a proinflammatory marker after cardiopulmonary bypass in children. J Thorac Cardiovasc Surg 2002; 123: 137-44.</mixed-citation></citation-alternatives></ref><ref id="cit12"><label>12</label><citation-alternatives><mixed-citation xml:lang="ru">Levy JH, Tanaka KA. Inflamatory response to cardiopulmonary bypass. Ann Thorac Surg 2003; 75: S715-20.</mixed-citation><mixed-citation xml:lang="en">Levy JH, Tanaka KA. Inflamatory response to cardiopulmonary bypass. Ann Thorac Surg 2003; 75: S715-20.</mixed-citation></citation-alternatives></ref><ref id="cit13"><label>13</label><citation-alternatives><mixed-citation xml:lang="ru">Maulik N, Yoshida T. Oxidative stress developed during open heart surgery induces inflammation: reduction of apoptotic cell death by ebselen a glutathione peroxidase mimic. J Cardiovasc Pharmacol 2000; 36: 601-8.</mixed-citation><mixed-citation xml:lang="en">Maulik N, Yoshida T. Oxidative stress developed during open heart surgery induces inflammation: reduction of apoptotic cell death by ebselen a glutathione peroxidase mimic. J Cardiovasc Pharmacol 2000; 36: 601-8.</mixed-citation></citation-alternatives></ref><ref id="cit14"><label>14</label><citation-alternatives><mixed-citation xml:lang="ru">Meyer K, Klocke RC, Schipke JD, et al. Ca2+ sensitizer superior to catecholamine during myocardial stunning? Eur J Card Thorac Surg 2008; 34: 326-31.</mixed-citation><mixed-citation xml:lang="en">Meyer K, Klocke RC, Schipke JD, et al. Ca2+ sensitizer superior to catecholamine during myocardial stunning? Eur J Card Thorac Surg 2008; 34: 326-31.</mixed-citation></citation-alternatives></ref><ref id="cit15"><label>15</label><citation-alternatives><mixed-citation xml:lang="ru">Moens AL, Claeys MJ, Timmermans JP, et al. Myocardial ischemia/ reperfusion- injury, a clinical view on a complex pathophysiological process. Int J Cardiol 2005; 100: 179-90.</mixed-citation><mixed-citation xml:lang="en">Moens AL, Claeys MJ, Timmermans JP, et al. Myocardial ischemia/ reperfusion- injury, a clinical view on a complex pathophysiological process. Int J Cardiol 2005; 100: 179-90.</mixed-citation></citation-alternatives></ref><ref id="cit16"><label>16</label><citation-alternatives><mixed-citation xml:lang="ru">Schmitt JP, Schroder J, Schunkert H, et al. Role of apoptosis in myocardial stunning after open heart surgery. Ann Thorac Surg 2002; 73: 1229-35.</mixed-citation><mixed-citation xml:lang="en">Schmitt JP, Schroder J, Schunkert H, et al. Role of apoptosis in myocardial stunning after open heart surgery. Ann Thorac Surg 2002; 73: 1229-35.</mixed-citation></citation-alternatives></ref><ref id="cit17"><label>17</label><citation-alternatives><mixed-citation xml:lang="ru">Sharma M, Ganguly NK, Chaturvedi G, et al. Release of proinflammatory mediators during myocardial ischemia/reperfusion injury in coronary artery bypass graft surgery. Molec Cell Biochem 2003; 247: 23-30.</mixed-citation><mixed-citation xml:lang="en">Sharma M, Ganguly NK, Chaturvedi G, et al. Release of proinflammatory mediators during myocardial ischemia/reperfusion injury in coronary artery bypass graft surgery. Molec Cell Biochem 2003; 247: 23-30.</mixed-citation></citation-alternatives></ref><ref id="cit18"><label>18</label><citation-alternatives><mixed-citation xml:lang="ru">Sherman SK. Perioperative myocardial ischemia reperfusion injury. Anesthesiol Clin N Amer 2003; 21: 465-85.</mixed-citation><mixed-citation xml:lang="en">Sherman SK. Perioperative myocardial ischemia reperfusion injury. Anesthesiol Clin N Amer 2003; 21: 465-85.</mixed-citation></citation-alternatives></ref><ref id="cit19"><label>19</label><citation-alternatives><mixed-citation xml:lang="ru">Sodha NR, Clements RT, Feng J, et al. The effects of therapeutic sulfide on myocardial apoptosis in response to ischemiareperfusion injury. Eur J Cardiothorac Surg 2008; 33: 906-13.</mixed-citation><mixed-citation xml:lang="en">Sodha NR, Clements RT, Feng J, et al. The effects of therapeutic sulfide on myocardial apoptosis in response to ischemiareperfusion injury. Eur J Cardiothorac Surg 2008; 33: 906-13.</mixed-citation></citation-alternatives></ref><ref id="cit20"><label>20</label><citation-alternatives><mixed-citation xml:lang="ru">Thielmann M, Dorge H, Martin C, et al. Myocardial dysfunction with coronary microembolization: signal transduction through a sequence of nitric jxide, tumor necrosis factor-alpha and sphingosine. Circ Res 2002: 90: 807-13.</mixed-citation><mixed-citation xml:lang="en">Thielmann M, Dorge H, Martin C, et al. Myocardial dysfunction with coronary microembolization: signal transduction through a sequence of nitric jxide, tumor necrosis factor-alpha and sphingosine. Circ Res 2002: 90: 807-13.</mixed-citation></citation-alternatives></ref><ref id="cit21"><label>21</label><citation-alternatives><mixed-citation xml:lang="ru">Triana JF, Li XY, Jamaluddin U, et al. Postischemic myocardial “stunned myocardium” identification of major differences between the open-chest and the conscious dog and evaluation of the oxygen radical hypothesis in the conscious dog. Circ Res 1991; 69: 731-47.</mixed-citation><mixed-citation xml:lang="en">Triana JF, Li XY, Jamaluddin U, et al. Postischemic myocardial “stunned myocardium” identification of major differences between the open-chest and the conscious dog and evaluation of the oxygen radical hypothesis in the conscious dog. Circ Res 1991; 69: 731-47.</mixed-citation></citation-alternatives></ref><ref id="cit22"><label>22</label><citation-alternatives><mixed-citation xml:lang="ru">Valen G. The basic biology of apoptosis and its implications for cardiac function and viability. Ann Thorac Surg 2003; 75: S656-60.</mixed-citation><mixed-citation xml:lang="en">Valen G. The basic biology of apoptosis and its implications for cardiac function and viability. Ann Thorac Surg 2003; 75: S656-60.</mixed-citation></citation-alternatives></ref><ref id="cit23"><label>23</label><citation-alternatives><mixed-citation xml:lang="ru">Wakaiyama H, Cowan DB, Toyoda Y, et al. Selective opening of mitochondrial ATP-Sensitive potassium channels during surgically induced myocardial ischemia decreases necrosis and apoptosis. Eur J Cardiothorac Surg 2002; 21: 424-33.</mixed-citation><mixed-citation xml:lang="en">Wakaiyama H, Cowan DB, Toyoda Y, et al. Selective opening of mitochondrial ATP-Sensitive potassium channels during surgically induced myocardial ischemia decreases necrosis and apoptosis. Eur J Cardiothorac Surg 2002; 21: 424-33.</mixed-citation></citation-alternatives></ref><ref id="cit24"><label>24</label><citation-alternatives><mixed-citation xml:lang="ru">Wang M, Crisostomo PR, Markel TA, et al. Mechanisms of sex differences in TNFR2- mediated cardioprotection. Circulation 2008; 118: S38-45.</mixed-citation><mixed-citation xml:lang="en">Wang M, Crisostomo PR, Markel TA, et al. Mechanisms of sex differences in TNFR2- mediated cardioprotection. Circulation 2008; 118: S38-45.</mixed-citation></citation-alternatives></ref><ref id="cit25"><label>25</label><citation-alternatives><mixed-citation xml:lang="ru">Wei GZ, Zhou JJ, Wang B, et al. Diastolic Ca2+ overload caused by Na+/Ca2+ exchanger during the first minutes of reperfusion results in continued myocardiol stunning. Eur J Pharmacol 2007; 572: 1-11.</mixed-citation><mixed-citation xml:lang="en">Wei GZ, Zhou JJ, Wang B, et al. Diastolic Ca2+ overload caused by Na+/Ca2+ exchanger during the first minutes of reperfusion results in continued myocardiol stunning. Eur J Pharmacol 2007; 572: 1-11.</mixed-citation></citation-alternatives></ref><ref id="cit26"><label>26</label><citation-alternatives><mixed-citation xml:lang="ru">Zeller CN, Wang Y, Markel TA, et al. Role of tumor necrosis factor receptor 1 in sex differences of stem cell mediated cardioprotection. Ann Thorac Surg 2009; 87: 812-9.</mixed-citation><mixed-citation xml:lang="en">Zeller CN, Wang Y, Markel TA, et al. Role of tumor necrosis factor receptor 1 in sex differences of stem cell mediated cardioprotection. Ann Thorac Surg 2009; 87: 812-9.</mixed-citation></citation-alternatives></ref><ref id="cit27"><label>27</label><citation-alternatives><mixed-citation xml:lang="ru">Zorc M, Vraspir-Porenta O, Zorc-Pleskovic R, et al. Apoptosis of myocites and proliferation markers as prognostic factors in end-stage dilated cardiomyopathy. Cardiovasc Pathol 2003; 12: 36-9.</mixed-citation><mixed-citation xml:lang="en">Zorc M, Vraspir-Porenta O, Zorc-Pleskovic R, et al. Apoptosis of myocites and proliferation markers as prognostic factors in end-stage dilated cardiomyopathy. Cardiovasc Pathol 2003; 12: 36-9.</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>
