Preview

Кардиоваскулярная терапия и профилактика

Расширенный поиск

Окислительный стресс – роль в патогенезе хронической сердечной недостаточности, возможности коррекции

https://doi.org/10.15829/1728-8800-2012-6-91-94

Аннотация

Сердечно-сосудистые заболевания (ССЗ) в течение многих лет являются лидирующей причиной смертности во всем мире. Согласно статистике Всемирной организации здравоохранения (ВОЗ), среди общей смертности в России смертность от ССЗ составляет 57%. В последние годы идут поиски новых маркеров ССЗ, которые могут улучшить диагностику и терапию этой обширной и прогностически неблагоприятной группы заболеваний. Значительные исследовательские усилия были направлены на выявление изменений в уровне маркеров окислительного стресса (ОС) и активности антиокислительных ферментов в качестве возможных механизмов, лежащих в основе развития ССЗ. Учитывая, что большое значение в последнее время придается плейотропным, в частности антиокислительным эффектам статинов, вопросы применения этого класса лекарств при хронической сердечной недостаточности (ХСН) активно обсуждаются медицинской общественностью в плане возможности их применения для лечения ХСН не только ишемической этиологии.

Об авторах

Л. О. Палаткина
Первый Московский государственный медицинский университет имени И. М. Сеченова, Москва
Россия
аспирант кафедры пропедевтики внутренних болезней


О. Н. Корнеева
Первый Московский государственный медицинский университет имени И. М. Сеченова, Москва
Россия
(контактное лицо) – врач-кардиолог


О. М. Драпкина
Первый Московский государственный медицинский университет имени И. М. Сеченова, Москва
Россия
зав.отделением кардиологии УКБ№ 2


Список литературы

1. Keith M, Geranmayegan A, Sole MJ, et al. Increased oxidative stress in patients with congestive heart failure. JACC 1998; 31: 1352-6.

2. Voyeykov V. L. Bio-physical and chemical aspects of aging and longevity. Successes of gerontology 2002; 9: 261. Russian (Воейков В.Л. Биофизико-химические аспекты старения и долголетия. Успехи геронтологии 2002; 9: 261).

3. Valko M, Morris H, Cronin MT. Metals, toxicity and oxidative stress. Curr Med Chem 2005; 12: 1161-208.

4. Drоge W. Free radicals in physiological control of cell function. Physiol Rev 2002; 82: 47–95.

5. Davies KJ. Oxidative stress: the paradox of aerobic life. Biochem Soc Symp. 1995; 61: 1–31.

6. McMurray J, Chopra M, Abdullah I, et al. Evidence of oxidative stress in chronic heart failure in humans. Eur Heart J 1993; 14: 1493– 8.

7. Higashi Y, Sasaki S, Nakagawa K, et al. Endothelial function and oxidative stress in renovascular hypertension. N Engl J Med 2002; 346: 1954-62.

8. Zotova I.V., Zateyshchikov D. A., Sidorenko B. A. Synthesis of nitric oxide and development of atherogenesis. Cardiology 2002; 4: 58-67. Russian (Зотова И.В., Затейщиков Д.А., Сидоренко Б.А. Синтез оксида азота и развитие атерогенеза. Кардиология 2002; 4: 58-67.)

9. Chen H, Hu CJ, He YY, et al. Reduction and restoration of mitochondrial dna content after focal cerebral ischemia/reperfusion. Stroke 2001; 32: 2382-7.

10. Xu J, Lupu F, Esmon C. Inflammation, innate immunity and blood coagulation. Hamostaseol 2010; 1. 30: 5–9.

11. Iyer A, Fairlie D, Prins J, et al. Inflammatory lipid mediators in adipocyte function and obesity. Nature Rev Endocrin 2010; 2. 6: 71–82.

12. Buggerand H, Abel D. Mitochondria in the diabetic heart. Cardiovascular Research 2010; 2. 88: 229–40.

13. Pankuweit S, Ruppert V, Maisch B. Inflammation in dilated cardiomyopathy. Herz 2004; 8. 29: 788–93.

14. Moreno P, Fuster V. New aspects in the pathogenesis of diabetic atherothrombosis. JACC 2004; 12. 44: 2293–300.

15. Seddon M, Looi H, Shah M. Oxidative stress and redox signalling in cardiac hypertrophy and heart failure. Heart 2007; 93: 903–7.

16. Davies KJ. Oxidative stress: the paradox of aerobic life. Biochem Soc Symp 1995; 61: 1–31.

17. Seshiah PN. Angiotensin II stimulation of NAD(P)H oxidase activity: upstream mediators. Circ Res 2002; 91: 406–13.

18. Sawyer DB. Role of oxidative stress in myocardial hypertrophy and failure. J Mol Cell Cardiol 2002; 34: 379–88.

19. Ungvari Z, Csiszar A, Huang A, et al. High pressure induces superoxide production in isolated arteries via proteinkinase C-dependent activation of NAD(P)H oxidase. Circulation 2003; 108: 1253-8.

20. Cave AC, Grieve DJ, Johar S, et al. NADPHoxidase-derived reactive oxygen species in cardiac pathophysiology. Philos Trans R Soc 2005; 360: 2327–34.

21. Landmesser U, Dikalov S, Price S. et al. Oxidation of tetrahydrobiopterin leads to uncoupling of endothelial cell nitricoxidesynthase in hypertension. J Clin Invest 2003; 8. 111: 1201–9.

22. Hill MF, Singal PK. Antioxidant and oxidative stress changes during heart failure subsequent to myocardial infarction in rats. Am J Pathol 1996; 148: 291-300.

23. Mallat Z, Philip I, Lebret M, et al. Elevated levels of 8-iso-prostaglandin in pericardial fluid of patients with heart failure: a potential role for in vivo oxidant stress in ventricular dilatation and progression to heart failure. Circulation 1998; 97: 1536–9.

24. Tsutsui H, Ide T, Hayashidani S, et al. Greaters usceptibility of failing cardiacmyocytes to oxygen free radical-mediated injury. Cardiovasc Res 2001; 49: 103-9.

25. Tsutamoto T, Wada A, Maeda K, et al. Attenuation of compensation of endogenous cardiac natriuretic peptide system in chronic heart failure: prognostic role of plasma brain natriuretic peptide concentration in patients with chronic symptomatic left ventricular dysfunction. Circulation. 1997; 96: 509–16.

26. Willenbrock R, Philipp S, Mitrovic V, et al. Neurohumoral blockade in CHF management. J Ren Angiot Aldoster Syst 2000; 1: 24–30.

27. Takano H, Hasegawa H, Nagai T, et al. Implication of cardiac remodeling in heart failure: mechanisms and therapeutic strategies. Intern Med 2003; 42: 465–9.

28. Tsutsui H, Kinugawa S, Matsushima S. Mitochondrial oxidative stress and dysfunction in myocardial remodelling. Cardiovasc Res 2009; 81: 449-56.

29. Siwik D, Pagano P, Colucci W. Oxidative stress regulates collagen synthesis and matrix metalloproteinase activity in cardiac fibroblasts. Am J Physiol 2001; 1. 280: 53–60.

30. Higuchi Y. Involvement of reactive oxygen species-mediated NF-kappa B activation in TNF-alpha-induced cardiomyocyte hypertrophy. J Mol Cell Cardiol 2002; 34: 233–40.

31. Thollon C, Iliou JP, Cambarrat С, et al. Nature of the cardiomyocyte injury induced by lipid hydroperoxides. Cardiovasc Res 1995; 30: 648–55.

32. Berlett BS, Stadtman ER. Protein oxidation in aging, disease, and oxidative stress. J Biol Chem 1997; 272: 203–6.

33. Wilson JR. Exercise in tolerance in heart failure. Importance of skeletal muscle. Circulation 1995; 91: 559-61.

34. Gao WD, Liu Y, Marban E. Selective effects of oxygen free radicals on excitationcontraction coupling in ventricular muscle: implications for the mechanism of stunned myocardium. Circulation 1996; 94: 2597–604.

35. Valko M, Leibfritz D, Mazur M. Free radicals and antioxidants in normal physiological functions and human disease. Intern J Biochem Cell Biol 2007; 1. 39: 44–84.

36. Vassalle C, Pratali L, Boni C, et al. An oxidative stress score as a combined measure of the pro-oxidant and anti-oxidant counterparts in patients with coronary artery disease. Clin Biochem 2008; 41: 1162-7.

37. Nordberg J, Arner E. Reactive oxygen species, antioxidants, and the mammalian thioredoxin system. Free Radic Biol Med 2001; 31: 1287–312.

38. The Heart Outcomes Prevention Evaluation Study Investigators. Vitamin E supplementation and cardiovascular events in high-risk patients. N Engl J Med 2000; 342: 154–60.

39. Heart Protection Study Collaborative G. MRC/BHF Heart Protection Study of antioxidant vitamin supplementation in 20 536 high-risk individuals: arandomised placebo-controlled trial. Lancet 2002; 360: 23–33.

40. Chopra M, McMurray J, Stewart J, et al. Free radical scavenging: a potentially beneficial action of thiol–containing angiotensin converting enzyme inhibitors. Biochem Soc Trans 1990; 18(6): 1184–5.

41. Сominacini L, Pasini A, Garbin U, et al. Zofenopril inhibits the expression of adhesion molecules on endothelial cells by reducing reactive oxygen species. Am J Hypertens 2002; 15(10): 891-5.

42. Pasini AF, Garbin U, Nava MC, et al. Effect of sulfhydryl and non–sulfhydryl angiotensin–converting enzyme inhibitors on endothelial function in essential hypertensive patients. Am J Hypertens 2007; 20(4): 443–50.

43. Cipollone F, Fazia M, Iezzi A, et al. Blockade of the angiotensin II type 1 receptor stabilizes atherosclerotic plaques in humans by inhibiting prostaglandin E2-dependent matrix metalloproteinase activity. Circulation 2004; 12. 109: 1482–8.

44. Celik T, Iyisoy A, Kursaklioglu H, et al. Comparative effects of nebivolol and metoprolol on oxidative stress, insulin resistance, plasma adiponectine and soluble P-selectine levels in hypertensive patients. J Hypertens 2006; 24: 591-6.

45. Dandona P, Ghanim H, Brooks D. Antioxidant activity of carvedilol in cardiovascular disease. J Hyperten 2007; 4. 25: 731–41.

46. Mason PR, Kalinowski L, et al. Nebivolol reduces nitroxidative stress and restores nitric oxide bioavailability in endothelium of black Americans. Circulation 2005; 112: 3795-801.

47. Belenkov YuN, Privalova EV, Danilogorskaya YuA, et al. Oxidative stress at a chronic heart failure. Possibilities of pharmacological correction. Cardiol Cardiovasc Surg 2009; 1: 4-9. Russian (Беленков Ю.Н., Привалова Е.В., Данилогорская Ю.А., и. др. Оксидативный стресс при хронической сердечной недостаточности. Возможности фармакологической коррекции. Кардиол серд.-сосуд хир 2009; 1: 4-9.)

48. Aronov DM. Application of statins in cardiological practice. Аttend Phys 2006; 9: 40-4. Russian (Аронов Д.М. Применение статинов в кардиологической практике. Леч врач 2006; 9: 40-4.)

49. Wassman S, Laufs U, Baumer AT, et al. HMG-CoA reductase inhibitors improve endothelial dysfunction in normocholesterolemic hypertension via reduced production of reactive oxygen species. Hypertension 2001; 37: 1450—7.

50. Hussein O, Schlezinger S, Rosenblat M, et al. Reduced susceptibility of low-density lipoprotein (LDL) to lipid peroxidation after fluvastatin therapy is associated with the hypocholesterolemic effect of the drug and its binding to the LDL. Atherosclerosis 1997; 128: 11–8.


Рецензия

Для цитирования:


Палаткина Л.О., Корнеева О.Н., Драпкина О.М. Окислительный стресс – роль в патогенезе хронической сердечной недостаточности, возможности коррекции. Кардиоваскулярная терапия и профилактика. 2012;11(6):91-94. https://doi.org/10.15829/1728-8800-2012-6-91-94

For citation:


Palatkina L.O., Korneeva O.N., Drapkina O.M. Oxidative stress, its role in the pathogenesis of chronic heart failure, and potential methods of correction. Cardiovascular Therapy and Prevention. 2012;11(6):91-94. (In Russ.) https://doi.org/10.15829/1728-8800-2012-6-91-94

Просмотров: 1108


Creative Commons License
Контент доступен под лицензией Creative Commons Attribution 4.0 License.


ISSN 1728-8800 (Print)
ISSN 2619-0125 (Online)