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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">glaucoma</journal-id><journal-title-group><journal-title xml:lang="ru">Национальный журнал Глаукома</journal-title><trans-title-group xml:lang="en"><trans-title>National Journal glaucoma</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">2078-4104</issn><issn pub-type="epub">2311-6862</issn><publisher><publisher-name>Federal State Budgetary Institution of Science “Krasnov Research Institute of Eye Diseases”</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.25700/NJG.2018.01.10</article-id><article-id custom-type="elpub" pub-id-type="custom">glaucoma-187</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>ОБЗОР ЛИТЕРАТУРЫ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>REVIEW OF LITERATURE</subject></subj-group></article-categories><title-group><article-title>СОСУДИСТАЯ ТЕОРИЯ ПАТОГЕНЕЗА ГЛАУКОМНОЙ ОПТИКОНЕЙРОПАТИИ: ОСНОВНЫЕ АСПЕКТЫ, ФОРМИРУЮЩИЕ СОСУДИСТУЮ ТЕОРИЮ ПАТОГЕНЕЗА ГЛАУКОМЫ. Часть 3</article-title><trans-title-group xml:lang="en"><trans-title>VASCULAR THEORY OF THE GLAUCOMATOUS OPTIC NEUROPATHY PATHOGENESIS: THE LEADING CONCEPTS OF VASCULAR THEORY. Part 3</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>Курышева</surname><given-names>Н. И.</given-names></name><name name-style="western" xml:lang="en"><surname>Kurysheva</surname><given-names>N. I.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Курышева Наталия Ивановна - доктор медицинских наук, профессор, руководитель консультативно-диагностического отдела </p><p>123098, Москва, ул. Гамалеи, 15</p></bio><bio xml:lang="en"><p>Med.Sc.D., Professor, Head of the Diagnostic Department </p><p>15 Gamalei st., Moscow, 123098</p></bio><email xlink:type="simple">e-natalia@list.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Центр офтальмологии ФМБА России, Клиническая больница № 86</institution><country>Россия</country></aff><aff xml:lang="en"><institution>The Ophthalmological Center of the Federal Medical and Biological Agency, Clinical Hospital No. 86</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2018</year></pub-date><pub-date pub-type="epub"><day>05</day><month>04</month><year>2018</year></pub-date><volume>17</volume><issue>1</issue><fpage>101</fpage><lpage>112</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Курышева Н.И., 2018</copyright-statement><copyright-year>2018</copyright-year><copyright-holder xml:lang="ru">Курышева Н.И.</copyright-holder><copyright-holder xml:lang="en">Kurysheva N.I.</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.glaucomajournal.ru/jour/article/view/187">https://www.glaucomajournal.ru/jour/article/view/187</self-uri><abstract><p>В данной части обзора представлены результаты клинических исследований, позволяющих предположить, что нарушение глазной гемодинамики может быть одним из пусковых факторов развития и прогрессирования глаукомы. Хотя факт первичности сосудистых нарушений при глаукоме все еще не доказан, существует рабочая концепция, допускающая их роль в патогенезе глаукомы. Она включает в себя теории венозной дисфункции, первичной сосудистой дисрегуляции и биомеханических нарушений на уровне решетчатой мембраны склеры. Так, при глаукоме имеется повышение пульсационного венозного давления, а отсутствие пульсации центральной вены сетчатки является неблагоприятным прогностическим признаком. В патогенезе глаукомы есть общие черты с окклюзиями вен сетчатки: для обоих характерна сосудистая дисрегуляция, касающаяся не только артериального, но и венозного русла. Окклюзия капилляров решетчатой мембраны склеры ослабляет как ее саму, так и проходящие через нее аксоны. Поскольку проблема циркуляторных расстройств при глаукоме находится в стадии обсуждения, на сегодняшний день отсутствуют четкие рекомендации по лечению, направленному на улучшение глазной гемодинамики при данной патологии. С учетом ауторегуляции глазного кровотока, действующей в широких пределах внутриглазного и перфузионного давления, назначение сосудистых препаратов с целью улучшения глазного кровотока проблематично.</p></abstract><trans-abstract xml:lang="en"><p>The review presents the results of clinical studies, which suggest that ocular hemodynamics disorder can be one of the triggers of glaucoma development and progression. While the fact that vascular disorders are primary in glaucoma still has not been proved, there is a working concept admitting their role in glaucoma pathogenesis. It includes a theory of venous dysfunction, primary vascular dysregulation and biomechanical disorders at the scleral membrane level. In glaucoma there is an increase in pulsatile venous pressure, and the lack of central retinal vein pulsation is an unfavorable prognostic. Glaucoma pathogenesis has some common features with retinal vein occlusion: both are characterized by vascular dysregulation, not only in arterial, but also venous bed. Occlusion of the scleral membrane’s capillaries weakens both the membrane and axons passing through it. Since the problem of circulatory disorders in glaucoma is still under discussion, currently there are no definitive treatment recommendations aimed at improving ocular hemodynamics in this disease. Taking into account that the ocular blood flow autoregulation is active in a wide range of IOP and perfusion pressure conditions, prescribing vasoactive drugs in order to improve the ocular blood flow is questionable.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>глаукома</kwd><kwd>глаукомная оптиконейропатия</kwd><kwd>глазной кровоток</kwd><kwd>гематоофтальмический барьер</kwd><kwd>задние цилиарные артерии</kwd><kwd>патогенез</kwd></kwd-group><kwd-group xml:lang="en"><kwd>glaucoma</kwd><kwd>glaucomatous optic neuropathy</kwd><kwd>ocular blood flow</kwd><kwd>hemato-ophthalmic barrier</kwd><kwd>posterior ciliary artery</kwd><kwd>pathogenesis</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">Hayreh S.S. Blood flow in the optic nerve head and factors that may influence it. 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