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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">microcirculation</journal-id><journal-title-group><journal-title xml:lang="ru">Регионарное кровообращение и микроциркуляция</journal-title><trans-title-group xml:lang="en"><trans-title>Regional blood circulation and microcirculation</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">1682-6655</issn><issn pub-type="epub">2712-9756</issn><publisher><publisher-name>Academician I.P. Pavlov First St. Petersburg State Medical University</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.24884/1682-6655-2026-25-3-91-97</article-id><article-id custom-type="elpub" pub-id-type="custom">microcirculation-1576</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>ОРИГИНАЛЬНЫЕ СТАТЬИ (ЭКСПЕРИМЕНТАЛЬНЫЕ ИССЛЕДОВАНИЯ)</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>ORIGINAL ARTICLES (EXPERIMENTAL INVESTIGATIONS)</subject></subj-group></article-categories><title-group><article-title>Протективные эффекты блокатора SGLT2 на морфо-функциональное состояние микрососудов кожи крыс при высокожировой алиментарной нагрузке</article-title><trans-title-group xml:lang="en"><trans-title>Protective Effects of the SGLT2 Blocker on the Morphofunctional State of Rat Skin Microvessels Under High-Fat Dietary Load</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-0188-5173</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Иванова</surname><given-names>Г. Т.</given-names></name><name name-style="western" xml:lang="en"><surname>Ivanova</surname><given-names>G. T.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Иванова Галина Тажимовна – канд. биол. наук, ведущий научный сотрудник лаборатории физиологии сердечно-сосудистой и лимфатической систем</p><p>199034, Санкт-Петербург, наб. Макарова, д. 6</p></bio><bio xml:lang="en"><p>Ivanova Galina T. – Candidate (PhD) in Biological sciences, leading researcher, laboratory of Physiology of the Cardiovascular and lymphatic systems</p><p>6, Makarova emb., Saint Petersburg, 199034 </p></bio><email xlink:type="simple">ivanovagt@infran.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0002-7532-2405</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Береснева</surname><given-names>О. Н.</given-names></name><name name-style="western" xml:lang="en"><surname>Beresneva</surname><given-names>O. N.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Береснева Ольга Николаевна – канд. биол. наук, старший научный сотрудник лаборатории клинической физиологии почек НИИ нефрологии НКИЦ</p><p>197022, Санкт-Петербург, ул. Льва Толстого, д. 6-8 </p></bio><bio xml:lang="en"><p>Beresneva Olga N. – Candidate (PhD) in Biological sciences, senior researcher, laboratory of Clinical renal Physiology, research institute of nephrology</p><p>6-8, L’va Tolstogo str., Saint Petersburg, 197022</p></bio><email xlink:type="simple">beresnevaolga@list.ru</email><xref ref-type="aff" rid="aff-2"/></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0003-3088-4647</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Лобов</surname><given-names>Г. И.</given-names></name><name name-style="western" xml:lang="en"><surname>Lobov</surname><given-names>G. I.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Лобов Геннадий Иванович – д-р мед. наук, профессор, заведующий лабораторией физиологии сердечно-сосудистой и лимфатической систем</p><p>199034, Санкт-Петербург, наб. Макарова, д. 6</p></bio><bio xml:lang="en"><p>Lobov Gennady I. – Doctor of medical sciences, Professor, Head, laboratory of Physiology of the Cardiovascular and lymphatic systems</p><p>6, Makarova emb., Saint Petersburg, 199034 </p></bio><email xlink:type="simple">lobovgi@infran.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Федеральное государственное бюджетное учреждение науки «Институт физиологии им. И. П. Павлова  Российской академии наук»</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Pavlov Institute of Physiology</institution><country>Russian Federation</country></aff></aff-alternatives><aff-alternatives id="aff-2"><aff xml:lang="ru"><institution>Федеральное государственное бюджетное образовательное учреждение высшего образования «Первый Санкт-Петербургский государственный медицинский университет имени академика И. П. Павлова» Министерства здравоохранения Российской Федерации</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Pavlov University</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2026</year></pub-date><pub-date pub-type="epub"><day>05</day><month>10</month><year>2026</year></pub-date><volume>25</volume><issue>3</issue><fpage>91</fpage><lpage>97</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Иванова Г.Т., Береснева О.Н., Лобов Г.И., 2026</copyright-statement><copyright-year>2026</copyright-year><copyright-holder xml:lang="ru">Иванова Г.Т., Береснева О.Н., Лобов Г.И.</copyright-holder><copyright-holder xml:lang="en">Ivanova G.T., Beresneva O.N., Lobov G.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.microcirc.ru/jour/article/view/1576">https://www.microcirc.ru/jour/article/view/1576</self-uri><abstract><sec><title>Введение</title><p>Введение. Увеличение распространенности ожирения и метаболических нарушений у людей требует поиска методов предупреждения осложнений со стороны сердечно-сосудистой системы, характерных для ассоциированных с метаболическими нарушениями заболеваний.</p><p>Цель – в эксперименте оценить возможный протективный эффект блокатора SGLT2 эмпаглифлозина (ЭМПА) на морфофункциональное состояние микрососудов кожи крыс, получавших избыточное количество жиров в диете.</p></sec><sec><title>Материалы и методы</title><p>Материалы и методы. Крысы групп ВЖР (n=12) и ЭМПА (n=12) в течение 8 недель содержались на высокожировом рационе (ВЖР, 50 % жира по калорийности). Крысам ЭМПА-группы также ежедневно вводили 1 мг/кг ЭМПА. Контролем служили крысы СР-группы (n=15), получавшие стандартный рацион (15 % жиров). После измерения артериального давления манжеточным методом у крыс исследовали кровоток в коже спины методом лазерной допплеровской флоуметрии, оценивали базовый показатель микроциркуляции и амплитуду его колебаний в эндотелиальном, нейрогенном и миогенном диапазонах, рассчитывали величину соответствующего тонуса. Реактивность микрососудистого русла кожи оценивали по величине прироста показателя микроциркуляции после ионофореза ацетилхолина (АХ) и нитропруссида натрия от базового. Определяли содержание триглицеридов, липопротеидов высокой и низкой плотности в крови, рассчитывали индекс массы висцерального жира. Количественную морфометрию микрососудов кожи выполняли в программе «Видео ТесТ-Морфология 5.2».</p></sec><sec><title>Результаты</title><p>Результаты. При ВЖР у крыс средний базовый показатель микроциркуляции уменьшался, тонус увеличивался во всех диапазонах, тогда как при применении ЭМПА тонус снижался. ЭМПА предотвращал подавление реактивности микрососудистого русла кожи: показатель микроциркуляции при действии АХ составлял 9,94±0,20 п. е. по сравнению с ВЖР-группой (8,12±0,18 п. е.), но был меньше, чем у СР-группы (10,65±0,22 п. е.). Дилатация на нитропруссид натрия была сходной с ВЖР и меньше чем у СР-группы. ЭМПА препятствовал увеличению толщины стенки микрососудов и предупреждал развитие фиброза, характерное для ВЖР.</p></sec><sec><title>Заключение</title><p>Заключение. Применение ЭМПА ослабляет эндотелиальную дисфункцию микрососудов кожи крыс при избыточном потреблении жиров, предупреждая снижение дилатации. ЭМПА уменьшает ремоделирование микрососудистой сети кожи при ВЖР.</p></sec></abstract><trans-abstract xml:lang="en"><sec><title>Introduction</title><p>Introduction. The increasing prevalence of obesity and metabolic disorders in humans necessitates the search for methods to prevent cardiovascular complications that are characteristic of diseases associated with metabolic disorders.</p><p>The objective of this study was to experimentally evaluate the potential protective effect of the sodium-glucose cotransporter 2 (SGLT2) blocker empagliflozin (EMPA) on the morphofunctional state of skin microvessels in rats fed a high-fat diet.</p></sec><sec><title>Materials and Methods</title><p>Materials and Methods. Rats in the high-fat diet (HFD) and EMPA groups (n=12 each) were maintained on the HFD (50 % fat) for 8 weeks. Rats in the EMPA group also received 1 mg/kg EMPA daily. Rats in the standard diet (SD) group (n=15), fed a standard diet (15 % fat), served as controls. After measuring blood pressure in rats by the cuff method, blood flow in the skin of the back was studied using laser Doppler flowmetry, the baseline microcirculation index and the amplitude of its fluctuations in the endothelial, neurogenic, and myogenic ranges was evaluated and the corresponding tone was calculated. The reactivity of the skin microvascular bed was assessed based on the increase in the microcirculation index after iontophoresis of acetylcholine (ACh) and sodium nitroprusside compared to the baseline. The blood levels of triglycerides, high-density and low-density lipoproteins were determined, and the visceral fat mass index was calculated. Quantitative morphometry of skin microvessels was performed using the Video Test-Morphology 5.2 program.</p></sec><sec><title>Results</title><p>Results. In rats on the HFD, the average baseline microcirculation index decreased, and the tone increased in all ranges, while the tone decreased when EMPA was applied. EMPA prevented the suppression of the reactivity of the skin microvascular bed: the microcirculation index in response to ACh was 9.94±0.20 p. u. in the EMPA group compared to the HFD group (8.12±0.18 p. u.), but it was lower than in the SD group (10.65±0.22 p. u.). The dilation response to sodium nitroprusside was similar to that of the HFD group and lower than that of the SD group. EMPA prevented an increase in microvessel wall thickness and prevented the development of fibrosis, which is typical for HFD.</p></sec><sec><title>Conclusion</title><p>Conclusion. EMPA application weakens endothelial dysfunction of the skin microvessels in rats with excessive consumption of fats, preventing a decrease in dilation. EMPA reduces remodeling of the microvascular network of the skin in HFD. </p></sec></trans-abstract><kwd-group xml:lang="ru"><kwd>лазерная допплеровская флоуметрия</kwd><kwd>микроциркуляция</kwd><kwd>метаболический синдром</kwd><kwd>морфометрия кожи</kwd><kwd>высокожировая диета</kwd><kwd>эмпаглифлозин</kwd><kwd>блокатор натрий-глюкозного котранспортера</kwd></kwd-group><kwd-group xml:lang="en"><kwd>laser Doppler flowmetry</kwd><kwd>microcirculation</kwd><kwd>metabolic syndrome</kwd><kwd>skin morphometry</kwd><kwd>high-fat diet</kwd><kwd>empagliflozin</kwd><kwd>sodium-glucose cotransporter blocker</kwd></kwd-group><funding-group><funding-statement xml:lang="ru">Работа поддержана средствами государственного задания ФГБУН «Институт физиологии им. И. П. Павлова РАН» (№ 1021062411787-0-3.1.8) и государственного задания ПСПбГМУ им. акад. И. П. Павлова (№ 121061700145-2).</funding-statement><funding-statement xml:lang="en">This work was supported by the state assignment of the I.P. Pavlov Institute of Physiology, Russian Academy of Sciences (No. 1021062411787-0-3.1.8) and the state assignment of Pavlov University (№ 121061700145-2).</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">Maccari R, Ottanà R. Sodium-glucose cotransporter inhibitors as antidiabetic drugs: current development and future perspectives. J Med Chem. 2022;65:10848–10881. Doi: 10.1021/acs.jmedchem.2c0086.</mixed-citation><mixed-citation xml:lang="en">Maccari R, Ottanà R. Sodium-glucose cotransporter inhibitors as antidiabetic drugs: current development and future perspectives. J Med Chem. 2022;65:10848–10881. Doi: 10.1021/acs.jmedchem.2c0086.</mixed-citation></citation-alternatives></ref><ref id="cit2"><label>2</label><citation-alternatives><mixed-citation xml:lang="ru">Raut S, Cucullo L. Antidiabetic agents as antioxidant and anti-inflammatory therapies in neurological and cardiovascular diseases. Antioxidants. 2025;14:1490. Doi: 10.3390/antiox14121490.</mixed-citation><mixed-citation xml:lang="en">Raut S, Cucullo L. Antidiabetic agents as antioxidant and anti-inflammatory therapies in neurological and cardiovascular diseases. Antioxidants. 2025;14:1490. Doi: 10.3390/antiox14121490.</mixed-citation></citation-alternatives></ref><ref id="cit3"><label>3</label><citation-alternatives><mixed-citation xml:lang="ru">Приходько В. А., Оковитый С. В., Куликов А. Н. Глифлозины при неалкогольной жировой болезни печени: перспективы применения за границами диабета, кардио- и нефропротекции // Терапия. 2023. Т. 9, № 7. С. 130–141. Doi: 10.18565/therapy.2023.7.130–141.</mixed-citation><mixed-citation xml:lang="en">Prikhodko VA, Okovity SV, Kulikov AN. Gliflozins in nonalcoholic fatty liver disease: prospects for use beyond diabetes, cardio- and nephroprotection. Therapy. 2023;9(7):130–141. (In Russ.)]. Doi: 10.18565/therapy.2023.7.130–141.</mixed-citation></citation-alternatives></ref><ref id="cit4"><label>4</label><citation-alternatives><mixed-citation xml:lang="ru">Shafiq A, Hameed I, Biegus J, et al. Empagliflozin in the treatment of heart failure. Future Cardiol. 2024;20 ( 5-6): 251–261. Doi: 10.1080/14796678.2024.2360818.</mixed-citation><mixed-citation xml:lang="en">Shafiq A, Hameed I, Biegus J, et al. Empagliflozin in the treatment of heart failure. Future Cardiol. 2024;20 ( 5-6): 251–261. Doi: 10.1080/14796678.2024.2360818.</mixed-citation></citation-alternatives></ref><ref id="cit5"><label>5</label><citation-alternatives><mixed-citation xml:lang="ru">Ivanova GT, Beresneva ON, Okovityi SV, et al. Effect of empagliflozin on reactivity of mesenteric arteries and skin microvessels in rats treated with doxorubicin. J Evol Biochem Phys. 2024;60 (Suppl 1):S196–S207. Doi: 10.1134/S0022093024070159.</mixed-citation><mixed-citation xml:lang="en">Ivanova GT, Beresneva ON, Okovityi SV, et al. Effect of empagliflozin on reactivity of mesenteric arteries and skin microvessels in rats treated with doxorubicin. J Evol Biochem Phys. 2024;60 (Suppl 1):S196–S207. Doi: 10.1134/S0022093024070159.</mixed-citation></citation-alternatives></ref><ref id="cit6"><label>6</label><citation-alternatives><mixed-citation xml:lang="ru">Ivanova GT, Beresneva ON, Khasun MH, et al. Effect of empagliflozin on the functional state of skin microcirculatory vessels in Wistar rats with kidney dysfunction. J Evol Biochem Phys. 2025;61(5):1620-1628. Doi: 10.1134/S0022093025050163.</mixed-citation><mixed-citation xml:lang="en">Ivanova GT, Beresneva ON, Khasun MH, et al. Effect of empagliflozin on the functional state of skin microcirculatory vessels in Wistar rats with kidney dysfunction. J Evol Biochem Phys. 2025;61(5):1620-1628. Doi: 10.1134/S0022093025050163.</mixed-citation></citation-alternatives></ref><ref id="cit7"><label>7</label><citation-alternatives><mixed-citation xml:lang="ru">Ivanova GT. Reactivity of mesenteric arteries in the development of metabolic syndrome in rats fed on a high-fat diet. J Evol Biochem Phys. 2023;59(1):154–164. Doi: 10.1134/S0022093023010131.</mixed-citation><mixed-citation xml:lang="en">Ivanova GT. Reactivity of mesenteric arteries in the development of metabolic syndrome in rats fed on a high-fat diet. J Evol Biochem Phys. 2023;59(1):154–164. Doi: 10.1134/S0022093023010131.</mixed-citation></citation-alternatives></ref><ref id="cit8"><label>8</label><citation-alternatives><mixed-citation xml:lang="ru">Oliva L, Aranda T, Caviola G, et al. In rats fed highenergy diets, taste, rather than fat content, is the key factor increasing food intake: a comparison of a cafeteria and a lipid-supplemented standard diet. Peer J. 2017;5:e3697. Doi: 10.7717/peerj.3697.</mixed-citation><mixed-citation xml:lang="en">Oliva L, Aranda T, Caviola G, et al. In rats fed highenergy diets, taste, rather than fat content, is the key factor increasing food intake: a comparison of a cafeteria and a lipid-supplemented standard diet. Peer J. 2017;5:e3697. Doi: 10.7717/peerj.3697.</mixed-citation></citation-alternatives></ref><ref id="cit9"><label>9</label><citation-alternatives><mixed-citation xml:lang="ru">Bushita H, Ozato N, Mori K, et al. Effect of visceral fat on onset of metabolic syndrome. Sci Rep. 2025;15(1):19012. Doi: 10.1038/s41598-025-01389-1.</mixed-citation><mixed-citation xml:lang="en">Bushita H, Ozato N, Mori K, et al. Effect of visceral fat on onset of metabolic syndrome. Sci Rep. 2025;15(1):19012. Doi: 10.1038/s41598-025-01389-1.</mixed-citation></citation-alternatives></ref><ref id="cit10"><label>10</label><citation-alternatives><mixed-citation xml:lang="ru">Engin A. Endothelial dysfunction in obesity and therapeutic targets. Adv Exp Med Biol. 2024;1460:489-538. Doi: 10.1007/978-3-031-63657-8.</mixed-citation><mixed-citation xml:lang="en">Engin A. Endothelial dysfunction in obesity and therapeutic targets. Adv Exp Med Biol. 2024;1460:489-538. Doi: 10.1007/978-3-031-63657-8.</mixed-citation></citation-alternatives></ref><ref id="cit11"><label>11</label><citation-alternatives><mixed-citation xml:lang="ru">Герасименко А. А., Петрушкина Ю. Н., Рыжов А. В. и др. Тромборезистентная функция эндотелия при ожирении // Регионарное кровообращение и микроциркуляция. 2025. Т. 24, № 4. С. 21–31. Doi: 10.24884/1682-6655-2025-24-4-21-31.</mixed-citation><mixed-citation xml:lang="en">Gerasimenko AA, Petrushkina YuN, Ryzhov AV, et al. Thromboresistant endothelial function in obesity. Regional blood circulation and microcirculation. 2025;24(4):21–31. (In Russ.)]. Doi: 10.24884/1682-6655-2025-24-4-21-31.</mixed-citation></citation-alternatives></ref><ref id="cit12"><label>12</label><citation-alternatives><mixed-citation xml:lang="ru">Seo MS, Jung HS, An JR, et al. Empagliflozin dilates the rabbit aorta by activating PKG and voltage-dependent K+ channels. Toxicol Appl Pharmacol. 2020;403:115153. Doi: 10.1016/j.taap.2020.115153.</mixed-citation><mixed-citation xml:lang="en">Seo MS, Jung HS, An JR, et al. Empagliflozin dilates the rabbit aorta by activating PKG and voltage-dependent K+ channels. Toxicol Appl Pharmacol. 2020;403:115153. Doi: 10.1016/j.taap.2020.115153.</mixed-citation></citation-alternatives></ref><ref id="cit13"><label>13</label><citation-alternatives><mixed-citation xml:lang="ru">Kloza M, Krzyżewska A, Kozłowska H, et al. Empagliflozin plays vasoprotective role in spontaneously hypertensive rats via activation of the SIRT1/AMPK pathway. Cells. 2025;14(7):507. Doi: 10.3390/cells14070507.</mixed-citation><mixed-citation xml:lang="en">Kloza M, Krzyżewska A, Kozłowska H, et al. Empagliflozin plays vasoprotective role in spontaneously hypertensive rats via activation of the SIRT1/AMPK pathway. Cells. 2025;14(7):507. Doi: 10.3390/cells14070507.</mixed-citation></citation-alternatives></ref><ref id="cit14"><label>14</label><citation-alternatives><mixed-citation xml:lang="ru">Zanchi A, Pruijm M, Muller ME, et al. Twenty-four hour blood pressure response to empagliflozin and its determinants in normotensive non-diabetic subjects. Front Cardiovasc Med. 2022;9:854230. Doi: 10.3389/fcvm.2022.854230.</mixed-citation><mixed-citation xml:lang="en">Zanchi A, Pruijm M, Muller ME, et al. Twenty-four hour blood pressure response to empagliflozin and its determinants in normotensive non-diabetic subjects. Front Cardiovasc Med. 2022;9:854230. Doi: 10.3389/fcvm.2022.854230.</mixed-citation></citation-alternatives></ref><ref id="cit15"><label>15</label><citation-alternatives><mixed-citation xml:lang="ru">Mroueh A, Algara-Suarez P, Fakih W, et al. SGLT2 expression in human vasculature and heart correlates with lowgrade inflammation and causes eNOS-NO/ROS imbalance. Cardiovasc Res. 2025;121(4):643–657. Doi: 10.1093/cvr/cvae257.</mixed-citation><mixed-citation xml:lang="en">Mroueh A, Algara-Suarez P, Fakih W, et al. SGLT2 expression in human vasculature and heart correlates with lowgrade inflammation and causes eNOS-NO/ROS imbalance. Cardiovasc Res. 2025;121(4):643–657. Doi: 10.1093/cvr/cvae257.</mixed-citation></citation-alternatives></ref><ref id="cit16"><label>16</label><citation-alternatives><mixed-citation xml:lang="ru">Cai C, Guo Z, Chang X, et al. Empagliflozin attenuates cardiac microvascular ischemia/reperfusion through activating the AMPKα1/ULK1/FUNDC1/mitophagy pathway. Redox Biol. 2022;52:102288. Doi: 10.1016/j.redox.2022.102288.</mixed-citation><mixed-citation xml:lang="en">Cai C, Guo Z, Chang X, et al. Empagliflozin attenuates cardiac microvascular ischemia/reperfusion through activating the AMPKα1/ULK1/FUNDC1/mitophagy pathway. Redox Biol. 2022;52:102288. Doi: 10.1016/j.redox.2022.102288.</mixed-citation></citation-alternatives></ref><ref id="cit17"><label>17</label><citation-alternatives><mixed-citation xml:lang="ru">d’Avila JC, Carlos AS, Vieira RL, et al. Beneficial effects of empagliflozin and liraglutide on the cerebral microcirculation of diabetic rats. Microcirculation. 2023;30(7):e12825. Doi: 10.1111/micc.12825.</mixed-citation><mixed-citation xml:lang="en">d’Avila JC, Carlos AS, Vieira RL, et al. Beneficial effects of empagliflozin and liraglutide on the cerebral microcirculation of diabetic rats. Microcirculation. 2023;30(7):e12825. Doi: 10.1111/micc.12825.</mixed-citation></citation-alternatives></ref><ref id="cit18"><label>18</label><citation-alternatives><mixed-citation xml:lang="ru">Mourmans SGJ, Achten A, Hermans R, et al. The effect of empagliflozin on peripheral microvascular dysfunction in patients with heart failure with preserved ejection fraction. Cardiovasc Diabetol. 2025;24(1):182. Doi: 10.1186/s12933-025-02679-8.</mixed-citation><mixed-citation xml:lang="en">Mourmans SGJ, Achten A, Hermans R, et al. The effect of empagliflozin on peripheral microvascular dysfunction in patients with heart failure with preserved ejection fraction. Cardiovasc Diabetol. 2025;24(1):182. Doi: 10.1186/s12933-025-02679-8.</mixed-citation></citation-alternatives></ref><ref id="cit19"><label>19</label><citation-alternatives><mixed-citation xml:lang="ru">Li H, Qin X, Zhang L, et al. Effect of SGLT2 inhibitors on inflammatory markers and oxygen consumption in non-diabetic patients with STEMI undergoing primary PCI: a parallel design single blind controlled trial. Heart Lung. 2025;73:174–179. Doi: 10.1016/j.hrtlng.2025.05.010.</mixed-citation><mixed-citation xml:lang="en">Li H, Qin X, Zhang L, et al. Effect of SGLT2 inhibitors on inflammatory markers and oxygen consumption in non-diabetic patients with STEMI undergoing primary PCI: a parallel design single blind controlled trial. Heart Lung. 2025;73:174–179. Doi: 10.1016/j.hrtlng.2025.05.010.</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>
