Tumo was associated with a hyperdynamic vasodilated state with increased biventricular performance. We postulate that tumo results in a massive increase in sympathetic activity with activation of brown adipose tissue and marked heat production. The increased heat production may explain the paradoxical vasodilatation in tumo practitioners exposed to subzero temperatures.
1 ФГБУН «ФИЦ питания и биотехнологии», Москва, Россия 2 ФГБОУ ВО "Российский национальный исследовательский медицинский университет имени Н.И. Пирогова", Москва, Россия 3 Городская клиническая больница №1 Департамента здравоохранения г. Москвы, РоссияОбоснование. Изучение молекулярно-генетических маркеров и патогенетических механизмов нейрогормональной активации, а также их значения в формировании сердечной недостаточности при ожирении является актуальной проблемой современной медицины, решение которой позволит осуществлять эффективную профилактику сердечно-сосудистых осложнений, оптимизировать лечение и улучшить прогноз пациентов с ожирением. Цель. Поиск генетических маркеров, предположительно вовлеченных в патогенез вторичной диастолической сердечной недостаточности (ДСН) у больных с ожирением. Методы. Проводилась диагностика методом полимеразной цепной реакции цельной крови 104 больных ожирением, которые были разделены на 2 группы в зависимости от наличия диастолической сердечной недостаточности. Анализировались следующие гены-кандидаты: ген ангиотензиногена AGT (C521T и T704C), ген рецептора ангиотензина II первого типа AGTR1 (A1166C), ген рецептора ангиотензина II второго типа AGTR2 (G1675A), ген альдостеронсинтазы CYP11B2 (C(-344)T). Результаты. Показано, что развитие вторичной ДСН у лиц с ожирением обоих полов ассоциируется с мутацией гена альдостеронсинтазы CYP11B2, а именно с заменой аллеля С в положении -344 на аллель Т и наличием генотипа Т/Т. Относительный риск развития заболевания при генотипе Т/Т повышен в 5,93 раза у мужчин (р=0,008) и в 4,57 раза у женщин (р=0,014). Для мужчин имеет значение мутация гена ангиотензиногена AGT, а именно замена аллеля C в положении 521 на аллель T. При этом относительный риск развития ДСН при генотипе Т/Т повышен в 4,26 раза (р=0,039). Мутации генов рецептора ангиотензина II первого типа AGTR1 (A1166C) и рецептора ангиотензина II второго типа AGTR2 (G1675A) не ассоциированы с развитием ДСН у больных с ожирением. Заключение. Представленные данные могут быть использованы при стратификации риска развития вторичной сердечной недостаточности у лиц с ожирением.КЛЮЧЕВЫЕ СЛОВА: сердечная недостаточность, ожирение, генетические полиморфизмы, ген ангиотензиногена AGT, ген рецептора ангиотензина II первого типа AGTR1, ген рецептора ангиотензина II второго типа AGTR2, ген альдостеронсинтазы CYP11B2. 3 First Graduate Hospital named after NI Pirogov, Moscow, Russia Background: the study of molecular genetic markers and pathogenetic mechanisms of neurohormonal activation, as well as their importance in the formation of heart failure in obesity, is an urgent problem of modern medicine, the solution of which will allow eff ective prevention of cardiovascular complications, optimize treatment and improve the prognosis of obese patients. Aims: search for genetic markers presumably involved in the pathogenesis of secondary diastolic heart failure in patients with obesity. Materials and methods: PCR-diagnostics of whole blood of 104 patients with obesity was carried out, which were divid...
Background. Among the goals of pathogenetic therapy in patients with multifocal atherosclerosis, not only control of the intensity of atherogenesis, but also the elastic properties of the arterial system is becoming increasingly important, which opens up additional ways to reduce overall and cardiovascular mortality in this category of patients. Aim. To evaluate effectiveness of medication Vazosponin (ZAO Vifitekh, Russia), which is a source of plant saponins in a dosage 400 mg per day, on the indicators of the elasticity of the great arteries. Materials and methods. The study included 100 patients with multifocal atherosclerosis: those who had had myocardial infarction or percutaneous coronary intervention during the previous 2 1 2 months and who had stenosing atherosclerosis of peripheral arteries brachiocephalic arteries and/or arteries of the lower extremities. The main group MG (n=50) consisted of patients who received combined hypolipidemic treatment: atorvastatin in dosage 40 mg/day + Vazosponin 400 mg/day along with baseline treatment. The control group (CG) included 50 patients who received only atorvastatin in dosage 40 mg/day along with baseline treatment. The observation period for each patient was 90 days with 3 control points (on the 1st, 10th and 90th days of therapy), in which were evaluated the elasticity indicators of the main arteries pulse wave velocity, linear blood flow velocity, total peripheral vascular resistance, actual specific vascular resistance. Results. There was a decrease in pulse wave velocity in both groups by the 90th day of the study, with a significant advantage in the group of patients who received Vazosponin: in the CG the indicator decreased by 7.3% (p0.05), in the MG by 19.3% (p0.05). The decrease in linear blood flow velocity was 14.3% (p0.05), in the CG the indicator decreased by 5.7% (p0.05). The dynamics of peripheral vascular resistance indicators showed an obvious advantage in the group of patients who received plant saponins: in the MG of patients, a decrease in total peripheral vascular resistance was detected by an average of 11.0% (p=0.006) and actual specific vascular resistance by 39.3% (p=0.0008), while in the CG by 4.5% and 5.0%, respectively. Conclusion. The addition of Vazosponin to the basic therapy of patients with multifocal atherosclerosis made it possible to achieve an additional increase in the elasticity of the arterial system, a significant decrease in peripheral vascular resistance, and the elimination of the escape effect of basic therapy. The data presented make it possible to consider the possibility of using preparations of plant saponins in combination therapy of patients with multifocal atherosclerosis who have instrumentally verified violations of the elastic properties of the arterial system.
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