Determinants of the respiratory system in hypertensive disease
- 作者: Smakotina S.A.1, Bazdyrev E.D.1, Rutkovskaya N.V.1, Barbarash O.L.1, Smakotina SA1, Bazdyrev ED1, Rutkovskaya NV1, Barbarash OL1
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- 期: 卷 82, 编号 9 (2010)
- 页面: 41-44
- 栏目: Editorial
- ##submission.dateSubmitted##: 09.04.2020
- ##submission.datePublished##: 15.09.2010
- URL: https://ter-arkhiv.ru/0040-3660/article/view/30654
- ID: 30654
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Subjects and methods. Forty-six hypertensive patients (mean age 43.2±4.0 years) were examined. Office blood pressure (BP) was measured. Electrocardiography, echocardiography, color Doppler ultrasonography of the brachial artery, 24-hour BP monitoring, spirography, body plethysmography, and study of the diffusion lung capacity for carbon monoxide were performed. The serum levels of interleukins 6, 8, and 10, tumor necrosis factor (TNF), and C-reactive protein (CRP) were measured.
Results. Inflammatory processes have been ascertained to contribute to the development and progression of HD. The increase in HD degree and stage is attended by a significant elevation of the plasma concentrations of proinflammatory cytokines, TNF, and CRP, which is due to the contribution of inflammatory processes in the vessel wall to the development of endothelial dysfunction, vascular remodeling, and organ lesions, including diminished lung function in HD.
Conclusion. Arterial hypertension, inflammatory indicators, endothelial function, and the degree of lesions to organs, including those in the respiratory system, are related. The basis for this relation is the common neurohumoral mechanisms of progression of nonspecific inflammation, endothelial dysfunction, and target organ lesions.
作者简介
Svetlana Smakotina
Email: smak67@mail.ru
Evgeniy Bazdyrev
Email: ebd624@mail.ru
Natal'ya Rutkovskaya
Ol'ga Barbarash
Email: olb61@mail.ru
S Smakotina
E Bazdyrev
N Rutkovskaya
O Barbarash
参考
- Дудко В. А., Карпов Р. С., Кляшев С. М. Сердце - легкие. Патогенез, клиника, функциональная диагностика и лечение сочетанных форм ишемической болезни сердца, хронических обструктивных болезней легких. Томск; 2004. 113-115.
- Гриппи М. А. Патофизиология легких. М.: Бином; 2005.
- Бродская Т. А., Невзорова В. А., Гельцер Б. И. Дисфункция эндотелия и болезни органов дыхания. / Тер. арх. 2007; 3: 76-84.
- Ефимов В. В., Блажко В. И., Воейкова Л. С. Показатели функции эндотелия у больных с ХОЗЛ различной степени тяжести. Укр. пульмонол. журн. 2005; 4: 44-47.
- Невзорова В. А., Зуга М. В., Гильцер Б. И. Роль окиси азота в регуляции легочных функций. Тер. арх. 1997; 3: 68-73.
- Guazzi M., Brambilla R. Diabetes worsens pulmonary diffusion in heart failure, and insulin counteracts this effect. Am. J. Respir. Crit. Care Med. 2002; 166: 978-982.
- Marshall R. P. The pulmonary renin-angiotensin system. Curr. Pharm. Design. 2003; 9(9): 715-722.
- Masmoudi K., Zouari N. Ventilatory mechanisms and alveolo-capillary diffusion in diabetes. Tunis Med. 2002; 80(9): 524- 530.
- Kim H., Cho H. O., Cho Y. K. et al. Relationship between early diastolic strain rate imaging and left ventricular geometric patterns in hypertensive patients. Heart Vessels 2008; 23(4): 271-278.
- Dorner T., Kiefer I., Kunze M. Gender aspects of socioeconomic and psychosocial risk factors of cardiovascular diseases. Wien. Med. Wschr. 2004; 154(17-18): 426-432.
- Howard D. C-reactive Protein and the Risk of Developing Hypertension / D. Howard. - www. JAMA. 2007.
- Карпов Ю. А., Сорокин Е. В. Атеросклероз и факторы воспаления: нелипидные механизмы действия статинов. Рус. мед. журн. 2001; 9(10): 43-51.
- Engstrom G., Lind P., Hedblad B. Lung function and cardiovascular risk relationship with inflammation-sensitive plasma proteins. Circulation 2002; 106: 2555-2660.
- Кобалава Ж. Д., Котовская Ю. В., Доготарь О. А. и др. Детерминанты воспалительного статуса и оксидативного стресса у больных с неосложненной артериальной гипертонией. Кардиоангиол. и ревматол. 2007; 1: 11-20.
- Armstrong L., Thickett D. R., Christie S. Increased expression of functionally active membrane-associated Tumor Necrosis Factor in acute Respiratory Distress syndrome. Am. J. Respir. Cell. Mol. Biol. 2000; 22(1): 68-74.
- Rissig L., Dimmeler S., Zeiher A. Apoptosis in the vascular wall and atherosclerosis. Basic Res. Cardiol. 2001; 96: 11-22.
- Schupp M., Janke J., Engeli S. Angiotensin type I receptor antagonists induce human in vitro adipogenesis through peroxicome proliferator-activated receptor-gamma activation. J. Hypertens. 2006; 24: 1809-1816.
- Кобалава Ж. Д., Котовская Ю. В., Хирманов В. Н. Артериальное давление в исследовательской и клинической практике. М.: Реафарм; 2004. 124-139, 316-325.
- Tsioufis C., Dimitriadis K., Chatzis D. et al. Relation of microalbuminuria to adiponectin and augmented C-reactive protein levels in men with essential hypertension. Am. J. Cardiol. 2005; 43: 791-796.
- Hillaert S., Van den Bossche W. Simultaneous determination of hydrochlorothiazide and several angiotensin II - receptor antagonist by capillary electrophoresis. J. Pharm. Biomed. Anal. 2003; 31: 329-339.
- Parissis J. T., Korovesis S., Giazitroglou E. et al. Plasma profiles of peripheral monocyte-related inflammatory markers in patients arterial hypertension. Correlations with plasma endothelin-I. Int. J. Cardiol. 2002; 83(1): 13-21.
- Abramson J. L., Weintraub W. S., Vaccarino V. Association between pulse pressure and C-reactive protein among apparently healthy US adults. J. Hypertens. 2002; 39: 197-202.
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