,, - [5, 11]., -, (NO)., NO,,. NO NO- (NOS). (nnos NOS1) (enos NOS3) NO-,, 2+- NO- (inos NOS2),,,,, [5]., NOS (nnos enos), inos. inos - ( ),, ( ),. NO
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1 , 70,9 ± 1,3% 58,0±0,86% /..,.. // today /.,..,.. //-.: -, /.., C. B.,.. [.] // C , - /..,.. // /..,.. // Mc Gurkin-Smith R. Reduction of intracanal bacteria using GT rotary instrumentation, 5,25% NaOCi, EDTA, and Ca(OH)2 / R. Mc Gurkin-Smith, M. Trope, D. Caplan // J. Endod Vol. 31. P :,, [ ]: THE STUDY OF THE RELATIVE OPTICAL DENSITY OF BONE IN THE TREATMENT OF CHRONIC APICAL GRANULOMATOUS PERIODONTITIS Zhdanova N. A. The results were evaluated in arbitrary units of optical density and bone density compared with optical median section tooth root on one radiograph. As a result of determining the relative bone density area periapical expected rate of destruction. Key words: optical density, point of reference, the rate of destruction.....,..,..,. -..., NO-,,,,. :,,,,. «-» ( 0115U001087). ( ), 30,.,,.
2 ,, - [5, 11]., -, (NO)., NO,,. NO NO- (NOS). (nnos NOS1) (enos NOS3) NO-,, 2+- NO- (inos NOS2),,,,, [5]., NOS (nnos enos), inos. inos - ( ),, ( ),. NOS- ' : -, 450,, ', L-, - (THB4), '. ;,, H (NADPH),. ' O2 L- - NO L- (. 1) [5, 9]. NO, / (RNS)., NO,,. NO (<1 ), enos nnos. NO,,, -, NO 450,, - [5, 13]., inos, NO (>1 M) (O2) (O2- ),, (N2O3) (OONO-) [7]., NO -.,. NO-. in vivo, ' 5 20 / ' inos (33±18% 9±2%) 3- (56±24% 0,3±0,4%) (p<0,05) [12]., 5 25 / 36
3 [10] inos, enos nnos [4]., inos,, NO (ONOO-).,,,,., - (O2- ). (O2- ) (H2O2) ( ),. O2- NO - (ONOO-). NO,,, (ONOO-) [7, 13]. NO NOS,, NOS,. NOS NO. NO, NO,, - [5].,, NO.,, -. ',,, N.,, [5, 8]. N,, - (O2- ), (H2O2), (N2O3) (OONO-). -., -, ,..., ECOG I-II,. 19 ( ) 64 ( ). Hoelzer. «7+3» «5+2» , 43 (51,8%), 40 (48,2%). 36 (43,4%), (61,1%), ( ), 14 (38,9%). ECOG IV;, ; IV,,,. 37
4 : (n=47) ; (n=36). 18 (10 8, 22,5±2,1 ). : ( ) / 2.. ( ) ( - ) [3]. ( ). [2]. NO - [NO2]- NOS, [NO2]- [6]... ( ),, (m). Pentium 5 Microsoft Office Excel 2007 (C ). <0, (53,19%) ;, 9 (19,1%).,. - 1,6 (p<0,01),. 2,3 ( <0,001) (. 1).,, -. NOS 3,9 ( 0,001), NOS [1]., -, NO, 1,2 ( >0,05),. 174,07±22,13 / 2, ( 4,12±1,2 ), 12 (25,5%) / ,,, NOS, * / (n=18) 8,16±0,51 0,94±0,034 3,2±0,38 0,61±0,08 (n=47) 13,1±1,42* 0,41±0,028* 2,7±0,41 2,4±0,11* (n=47) 17,9±1,09* 0,46±0,031* 2,2±0,26* 2,42±0,10* : * (p<0,05); / 2 ( <0,05). 38
5 -,, 1,4 ( <0,02). (0,46±0,031 / 0,41±0,028 / ; <0,05),,,,. NOS 2,42 *, 1,45 ( <0,05) 1,2 ( >0,05) (.1). NOS,. 29 (80,5%), 7 (41,6%),. - 2,1 ( <0,05) (. 2) 2,8 ( <0,05).,. NOS 3,8 ( 0,001) - 1,5 ( 0,05)., NO,. (162,04±24,65 / 2)., 26 (72,2%), 19 (52,8%), 11 (30,5%). 7,12±0, ,, /, NOS, * (n=18) 8,16±0,51 0,94±0,034 3,2±0,38 0,61±0,08 (n=36) 17,1±1,57* 0,34±0,021* 2,18±0,31* 2,3±0,14* (n=36) 22,8±1,98* 0,29±0,019* 1,8±0,21* 1,97±0,13* - 1,3 ( <0,05).,. 2,7 ( <0,001) (0,34±0,021 / 0,29±0,019 / ; >0,05) (. 2). NOS, NOS. 1,8 - ( <0,01) 1,2 ( >0,05) (. 2),,, / 2,.,, 39
6 , ( ) 550 / /..,..,.. [.] //.... :, L- - /.. // , /..,.. /.:, Aldieri E. Doxorubicin induces an increase of nitric oxide synthesis in rat cardiac cells that is inhibited by iron supplementation / E. Aldieri, L. Bergandi, C. Riganti [et al.] // Toxicol. Appl. Pharmacol Vol P Fogli S. The role of nitric oxide in anthracycline toxicity and prospects for pharmacologic prevention of cardiac damage / S. Fogli, P. Nieri, M.C. Breschi // FASEB J Vol. 18. P Hevel J.M. Purification of the inducible murine macrophage nitric oxide synthase / J.M. Hevel // J. Biol. Chem Vol. 266, N34. P Jungsuwadee P. Doxorubicin-induced cardiomyopathy: an update beyond oxidative stress and myocardial cell death / P. Jungsuwadee // Cardiovasc. Regen. Med Vol p. 8. Lymanets T. The free radical oxidation role in the development of anthracycline-induced cardiotoxicity in patients with acute leukemia in the presence of concomitant ischemic heart disease / T. Lymanets, I. Skrypnyk, G.Maslova // Hematologica Vol. 100, Suppl.1. P Mungrue I.N. The role of NOS in heart failure: lessons from murine genetic models / I.N. Mungrue, M. Husain, D.J. Stewart // Heart Fail. Rev Vol. 7. P Pacher P. Potent metalloporphyrin peroxynitrite decomposition catalyst protects against the development of doxorubicininduced cardiac dysfunction / P.Pacher, L. Liaudet, P.Bai [et al.] // Circulation Vol P Raj S. Anthracycline-induced cardiotoxicity: a review of pathophysiology, diagnosis and treatment / S. Raj, V.I. Franco, S.E. Lipshultz // Curr. Treat. Options Cardiovasc. Med Vol. 16. P Weinstein D. M. Cardiac peroxynitrite formation and left ventricular dysfunction following doxorubicin treatment in mice / D.M. Weinstein, M.J. Mihm, J.A. Bauer // J. Pharmacol. Exp. Ther Vol P Zhu S.-G. Dietary nitrate supplementation protects against doxorubicin-induced cardiomyopathy by improving mitochondrial function / S.-G. Zhu, R.C.Kukreja, A. Das [et al.] // J. Am. Coll. Cardiol Vol. 57. P ,.., , NO-,,,,. :,,,, THE NITRIC OXIDE SYSTEM IMBALANCE ROLE IN THE DEVELOPMENT OF ANTHRACYCLINE CARDIOTOXICITY IN ACUTE LEUKEMIA PATIENTS WITH CONCOMITANT ISCHEMIC HEART DISEASE Lymanets T. V., Maslova G. S., Skrypnyk I. M. The article presents the own researches results of the leading pathogenetic ways determining of anthracycline-induced cardiotoxicity formation in patients with acute leukemia, depending on the presence of concomitant ischemic heart disease (IHD). The activation of aggressive oxygen species production is observed in all patients at the onset of acute leukemia with simultaneous antioxidant protection exhaustion. These processes are enhanced in the chemotherapy dynamics. In addition, there is an increased activity of summary NO-synthase in all patients with acute leukemia, that only in case of concomitant IHD is accompanied with the development of endothelial dysfunction, which creates conditions for deepening violations in the system of nitric oxide and consequently leads to heart tissue injury on a background of anthracycline antibiotics accumulation. Key words: acute leukemia, ischemic heart disease, anthracycline cardiotoxicity, nitric oxide, endothelial dysfunction... 40
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