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<article 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" xmlns:ali="http://www.niso.org/schemas/ali/1.0/" article-type="other" dtd-version="1.2" xml:lang="en"><front><journal-meta><journal-id journal-id-type="publisher-id">Journal of Experimental and Clinical Surgery</journal-id><journal-title-group><journal-title xml:lang="en">Journal of Experimental and Clinical Surgery</journal-title><trans-title-group xml:lang="ru"><trans-title>Вестник экспериментальной и клинической хирургии</trans-title></trans-title-group></journal-title-group><issn publication-format="print">2070-478X</issn><issn publication-format="electronic">2409-143X</issn><publisher><publisher-name xml:lang="en">Voronezh State Medical University named after N.N. Burdenko</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="publisher-id">69</article-id><article-id pub-id-type="doi">10.18499/2070-478X-2014-7-2-109-114</article-id><article-categories><subj-group subj-group-type="toc-heading" xml:lang="en"><subject>Original articles</subject></subj-group><subj-group subj-group-type="toc-heading" xml:lang="ru"><subject>Оригинальные статьи</subject></subj-group><subj-group subj-group-type="article-type"><subject>Unknown</subject></subj-group></article-categories><title-group><article-title xml:lang="en">The Role of Microsomal-Monooxygenase System of Liver and Indirect Electrochemical Oxidation of Blood in the Formation Mechanism of Endogenous Intoxication Syndrome in Animals with Experimental Bile Peritonitis</article-title><trans-title-group xml:lang="ru"><trans-title>Роль микросомально-монооксигеназной системы печени и непрямого электрохимического окисления крови в механизме формирования синдрома эндогенной интоксикации у животных с экспериментальным желчным перитонитом</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author"><name><surname>Рыкунова</surname><given-names>В.Е.</given-names></name><address><country country="RU">Russian Federation</country></address><bio xml:lang="en"><p>postgraduate of the department of operative surgery and topographic anatomy of the Kuban State Medical University.</p></bio><bio xml:lang="ru"><p>аспирант кафедры оперативной хирургии и топографической анатомии Кубанского государственного медицинского университета</p></bio><email>author@vestnik-surgery.com</email><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><name><surname>Терещенко</surname><given-names>О.А.</given-names></name><address><country country="RU">Russian Federation</country></address><bio xml:lang="en"><p>PhD, assistant of the department of operative surgery and topographic anatomy, State educational state-funded institution of higher professional education of the Kuban State Medical University.</p></bio><bio xml:lang="ru"><p>к.м.н., асс. кафедры оперативной хирургии и топографической анатомии Кубанского государственного медицинского университета</p></bio><email>author@vestnik-surgery.com</email><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><name><surname>Петросян</surname><given-names>Е.А.</given-names></name><address><country country="RU">Russian Federation</country></address><bio xml:lang="en"><p>MD, Professor of operative surgery and topographical anatomy, State educational state-funded institution of higher professional education of the Kuban State Medical University. E-mail: superego_ksmu@mail.ru.</p></bio><bio xml:lang="ru"><p>д.м.н., проф. кафедры оперативной хирургии и топографической анатомии Кубанского государственного медицинского университета</p></bio><email>superego_ksmu@mail.ru</email><xref ref-type="aff" rid="aff1"/></contrib></contrib-group><aff-alternatives id="aff1"><aff><institution xml:lang="en">Kuban State Medical University, 4 Sedina Str., Krasnodar, 350063, Russian Federation</institution></aff><aff><institution xml:lang="ru">Кубанский государственный медицинский университет, ул. Седина, д. 4, Краснодар, 350063, Российская Федерация</institution></aff></aff-alternatives><pub-date date-type="pub" iso-8601-date="2014-06-24" publication-format="electronic"><day>24</day><month>06</month><year>2014</year></pub-date><volume>7</volume><issue>2</issue><issue-title xml:lang="ru"/><fpage>109</fpage><lpage>114</lpage><history><date date-type="received" iso-8601-date="2016-04-26"><day>26</day><month>04</month><year>2016</year></date><date date-type="accepted" iso-8601-date="2016-04-26"><day>26</day><month>04</month><year>2016</year></date></history><permissions><copyright-statement xml:lang="en">Copyright ©; 2014, ., ., .</copyright-statement><copyright-statement xml:lang="ru">Copyright ©; 2014, Рыкунова В., Терещенко О., Петросян Е.</copyright-statement><copyright-year>2014</copyright-year><copyright-holder xml:lang="en">., ., .</copyright-holder><copyright-holder xml:lang="ru">Рыкунова В., Терещенко О., Петросян Е.</copyright-holder><ali:free_to_read xmlns:ali="http://www.niso.org/schemas/ali/1.0/"/><license><ali:license_ref xmlns:ali="http://www.niso.org/schemas/ali/1.0/">http://creativecommons.org/licenses/by-nc-nd/4.0</ali:license_ref></license></permissions><self-uri xlink:href="https://vestnik-surgery.com/journal/article/view/69">https://vestnik-surgery.com/journal/article/view/69</self-uri><abstract xml:lang="en"><p>Relevance On the background of growth in the number of patients JCB problem ha is of particular relevance. Ha leads to the development of systemic inflammatory response, which is accompanied by excessive generation of cytokines, are able to inhibit the activity of cytochrome P-450-dependent MOS liver, responsible for the biotransformation of endogenous compounds. The purpose of the study Is to evaluate the modulating effect NGH on MOS liver in experimental. Materials and methods Study of cytochrome P-450-dependent MOS liver conducted on 120 mongrel rats-males, weighing 160-200, by the method of A.I. Archakov (1975) and I.I. Carosino et al., (1977). The protein content in a fraction of microsomes determined by O. Lowry (1951). The number of microsomal cytochrome P-450 were determined by the method of T. Omura, R. Sato (1964). State MOS liver was estimated by the rate N-demethylation of antipyrine and gidrauxilirovania aniline (I.I. Karuzina, A.I. Archakov, 1977). Results and their discussion Experiments indicate the development of the syndrome of EI in animals with ha oppression antitoxic function of the liver. Introduction of 0.03% solution NGH causes a significant increase of cytochrome P-450 and b5, indicating that it permantently activity, at the same time as the use of 0.1% solution NGH causes a decrease of their content, indicating fermentarii effect. Conclusion Obtained result is of considerable clinical importance, because the biotransformation of many of the antibiotics used in the treatment of acute abdominal pathology occurs almost exclusively microsomal enzymes hepatocytes that against bacterial infection there is a significant risk of overdose, therefore, the use of 0.03% solution NGH can contribute to the induction of cytochrome P450 liver</p></abstract><trans-abstract xml:lang="ru"><p>Актуальность На фоне роста количества больных желчнокаменной болезнью проблема желчного перитонита (ЖП) представляет особую актуальность. ЖП приводит к развитию системного воспалительного ответа, который сопровождается избыточной генерацией цитокинов, способных угнетать активность цитохром Р-450-зависимых монооксигеназ печени, ответственных за биотрансформацию эндогенных соединений. Цель исследования Оценка модулирующего действия натрия гипохлорита (НГХ) на микросомально-монооксигеназную систему (МОС) печени при экспериментальном ЖП. Материалы и методы Исследование цитохром Р-450-зависимой МОС печени проведены на 120 беспородных крысах-самцах, массой 160-200 г. по методике А.И. Арчакова (1975) и И.И. Карузиной с соавт., (1977). Содержание белка во фракции микросом определяли по О. Lowry (1951). Количество микросомального цитохрома Р-450 определяли по методу T. Omura, R. Sato (1964). Состояние МОС печени оценивали по скорости N-деметилирования антипирина и гидроксилирования анилина (И.И. Карузина, А.И. Арчаков, 1977). Результаты и их обсуждение Результаты экспериментов свидетельствуют о развитии синдрома эндогенной интоксикации у животных с ЖП, с угнетением антитоксической функции печени. Введение 0,03% раствора НГХ вызывает достоверное увеличение цитохрома Р-450 и b5, что свидетельствует о его ферментиндуцирующей активности, в то время, как применение 0,1% раствора НГХ вызывает снижение их содержания, что указывает на ферментингибирующий эффект. Заключение Полученный результат имеет существенное клиническое значение, так как биотрансформация многих антибиотиков, используемых при лечении острой абдоминальной патологии, происходит почти исключительно микросомальными ферментами гепатоцитов, в связи с чем на фоне бактериальной инфекции имеется существенный риск их передозировки. Применение 0,03% раствора НГХ может способствовать индуцированию цитохрома Р450 печени.</p></trans-abstract><kwd-group xml:lang="en"><kwd>сholeperitonitis</kwd><kwd>microsomal-monooxygenase system of the liver</kwd><kwd>sodium hypochlorite</kwd></kwd-group><kwd-group xml:lang="ru"><kwd>желчный перитонит</kwd><kwd>микросомальномонооксигеназная система печени</kwd><kwd>натрия гипохлорит</kwd></kwd-group><funding-group/></article-meta></front><body></body><back><ref-list><ref id="B1"><label>1.</label><mixed-citation>1. Archakov A. I. Mikrosomal'nogo okisleniya. [Microsomal oxidation.] M.:Nauka, 1975; p. 327</mixed-citation></ref><ref id="B2"><label>2.</label><mixed-citation>2. Botashev A. A., the Landlord, Yu., Tereshchenko O. A., etc. Rol' markerov disfunkcii ehndoteliya sosudov pri abdominal'nom sepsise zhelchnogo proiskhozhdeniya. Infekcii v hirurgii. [the Role of markers of endothelial dysfunction of the vessels in the abdominal sepsis biliary origin. 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