The dynamics of biochemical markers of re-modulating of myocardium in children with dilation cardiomyopathy against the background of complex therapy
Tatyana V. Bershova , M. I Bakanov , E. N Basargina , A. G Gasanov , A. P Ivanov , S. V Monaenkova
Russian Medicine ›› 2014, Vol. 20 ›› Issue (5) : 25 -29.
The dynamics of biochemical markers of re-modulating of myocardium in children with dilation cardiomyopathy against the background of complex therapy
The development of methods of treatment of chronic cardiac insufficiency under dilation cardiomyopathy in children is an actual issue of children cardiology. The article presents complex clinical biochemical results of examination of children with chronic cardiac insufficiency under dilation cardiomyopathy. the complex therapy included inhibitors of angiotensin converting enzyme and P-adrenoceptor antagonists. On the basis of analysis in blood serum concentrations of matrix metalloproteinase, matrix metalloproteinase tissue inhibitor-1, content of single components of apoptosis, superoxide dismutase and total nitrogen oxide the alterations of these biologically active agents in blood serum of children with different stage of circulatory disturbance prior and after application of cardio-protection therapy. It is demonstrated that amelioration of clinical conditions of patients with circulatory disturbance stage I-IIA is followed by tendency to normalization of content of matrix metalloproteinase, matrix metalloproteinase tissue inhibitor-1 and decreasing of degree of apoptosis cell destruction. This trend can be caused by capacity of inhibitors of angiotensin converting enzyme and P-adrenoceptor antagonist to suppress increased synthesis of matrix metalloproteinase and processes of apoptosis due to decreasing of degree of hypoxic damage of cardiac hystiocytes. In children with circulatory disturbance stage IIB-III resistance to the applied therapy can be a consequence of increased endogenous production of nitrogen oxide.
matrix metalloproteinase / apoptosis / nitrogen oxide / superoxide dismutase / circulatory insufficiency
| [1] |
Капелько В.И. Внеклеточный матрикс миокарда и его изменения при заболеваниях сердца. Кардиология. 2000; 40(9): 78-90. |
| [2] |
Hsu D.T., Pearson G.D. Heart failure in childern history, etiology and pathophysiology. J. Circ. Heart Fail. 2009; 2: 63-70. |
| [3] |
Nagase H., Woessner J.F.Jr. Matrix metalloproteinases. J. Biol. Chem. 1999; 274(31): 21491-4. |
| [4] |
Yamamoto D., Takai S., Miyazaki M. Inhibitory profiles of captopril on matrix metalloproteinase-9 activity. Eur. J. Pharmacol. 2008; 588(2-3): 277-9. |
| [5] |
Li Y., Takemura G., Kosai K. et al. Critical roles for the fas/fas ligand system in postinfarction ventricular remodeling and heart failure. Circ. Res. 2004; 95(6): 627-36. |
| [6] |
Белушкина Н.Н., Северин С.Е. Молекулярные основы патологии апоптоза. Архив патологии. 2001; 63(1): 51-9. |
| [7] |
Gibbons G.H. Endothelial function as a determinant of fascular function and structure f new therapeutic target. Am. J. Cardiol. 1997; 79: 3-8. |
| [8] |
Национальные рекомендации Всероссийского научного общества и Общества специалистов кардиологов по хронической сердечной недостаточности. (II пересмотр). Сердечная недостаточность. 2007; 8(2). |
| [9] |
Schnee J.M., Hsueh W.A. Angiotensin II, adhesion, and cardiac fibrosis. Cardiovasc. Res. 2000; 46: 264-8. |
| [10] |
Chow A.K., Cena J., Schulz R. Acute actions and novel targets of matrix metalloproteinases in the heart and vasculature. Br. J. Pharmacol. 2007; 152: 189-205. |
| [11] |
Окунева Г.Н., Чернявский А.М., Левичева Е.Н. и др. Распределение химических элементов в разных отделах сердца больных ишемической болезнью сердца с острой сердечной недостаточностью. Кардиология. 2008; 48(2): 41-6. |
| [12] |
Hayashi T., Elfering S., Traaseth N., Giulivi C. Mitochondrial nitricoxyde synthase: enzyme expression, characterization, fnd regulation. J. Bioeuerg. Biomembr. 2004; 36: 341-6. |
| [13] |
Han W., Fu S., Wei N. et al. Nitric oxide overproduction derived from inducible nitric oxide synthase increases cardiomyocyte apoptosis in human atrial fibrillation. In. J. Cardiol. 2008; 130(2): 165-73. |
| [14] |
Spinale F.G. Myocardial matrix remodeling and the matrix metalloproteinases: influence on cardiac form and function. Physiol. Rev. 2007; 87: 1285-342. |
| [15] |
Richard P., Villard T., Charron P. The genetic bases of cardiomyopathies. J. Am. Coll. Cardiol. 2006; 48(9): A79-89. |
Eco-Vector
/
| 〈 |
|
〉 |