Efficacy of different cardiotonic drug on severity of endotoxemia under heart failure coupled with systemic inflammatory syndrome in experiments
Abstract
On the model of systemic inflammatory response syndrome caused by toxi-allergic myocarditis 10-day duration in rabbits the efficacy of 5 days (beginning after 5 days from the injection of staphylococcus toxins) administration of the various pharmacological agents on the endotoxemia intensity has been studied. It has been shown that pathological shifts in cytokine system in myocardium occurs early than in blood. The efficacy of action of the studding cardiotonic drug on the endotoxemia were: Adenocin® > amrinone ≥ digoxin > levosimendan. Influence of Adenocin®, and in less extent digoxin unlike amrinone and levosimendan, leads to the decreasing in the expression of nuclear transcription factor NF-kB and expression of intercellular adhesion molecule-1 (ICAM-1).
About the Authors
D. I. Ionov
Kuban state medical university
Russian Federation
Russian Federation
M. M. Fedorova
Russian academy of postgraduate study ministry of health and social development
Russian Federation
Russian Federation
G. V. Sukoyan
International scientific-research centre of introduction and development of new biomedical technology
Russian Federation
Russian Federation
P. A. Galenko-Yaroshevsky
Kuban state medical university
Russian Federation
Russian Federation
N. V. Gongadze
International scientific-research centre of introduction and development of new biomedical technology
Russian Federation
Russian Federation
References
1. Бокерия Л.А., Маликов В.Е., Арзуманян М.А. и др. Рациональная фармакокоррекция синдрома системного воспалительного ответа у больных ишемической болезнью сердца со сниженнной сократительной функцией сердца // Бюллетень НЦССХ им. А.Н. Бакулева РАМН. - 2008. - № 3. -С. 85-92.
2. Лейдерман И.Н. Синдром полиорганной недостаточности // Вестник интенсивной терапии. - 1999. - № 3. - С. 19-20.
3. Сукоян Г.В., Антелава Н.А. Рациональная фармакоррекция синдрома системного воспалительного ответа при тяжелой сердечной недостаточности // Бюл. экспер. биол. -2009. - № 4. - С. 411-414.
4. Сукоян Г.В., Гонгадзе Н.В. Механизм кардиопротекторного действия аденоцина и кардиотонических средств негликозидной природы при хронической недостаточности сердца в эксперименте // Бюл. экспер. биол. - 2010. - № 11. - С. 541-544.
5. Чаленко В.В., Катушев Ф.Х. Эндогенная интоксикация в хирургии // Вест. хир. им. И.И. Грекова. - 1990. - № 4. -С. 3-8.
6. Chanani N.K., Cowan D.B., Takeuchi K. et al. Differential effects of amrinone and milrinone upon myocardial inflammatory signaling // Circulation. - 2002. - Vol. 106 (suppl. 1). -P. 284-289.
7. de Vasconcelos D.I.B,, Leite J.A., Carneiro L.T. et al. Anti-inflammatory and antinociceptive activity of ouabain in mice // Mediators of Inflammation. - 2011. - № 2011 (11).
8. Hasko G., Sitkovsky M.V., Szabo C. Immunomodulatory and neuroprotective effects of inosine // TRENDS in pharmacological Sciences. - 2004. - Vol. 25 (3). - P. 152-157.
9. Iwasaki A., Matsumori A., Yamada T. et al. Pimobendan inhibits the production of proinflammatory cytokines and gene expression of inducible nitric oxide synthase in a murine model of viral myocarditis // J. am. col. cardiol. - 1999. - Vol. 33. -P. 1400-1407.
10. Matsumori A., Ono K., Nishio R., et al. Modulation of cytokine production and protection against lethal endotoxemia by the cardiac glycoside ouabain // Circulation. - 1997. - Vol. 96. -P. 1501-1506.
11. Mazumdar K., Ganguly K., Kumar K.A. et al. Antimicrobial potentiality of a new non-antibiotic: the cardiovascular drug oxyfedrine hydrochloride // Microbiological res. - 2003. -Vol. 158 (3). - P. 259-264.
12. Nascimento F.P., Figueredo S.M., Marcon R. et al. Inosine reduces pain-related behaviour in mice involvement of adenosine A1 and A2A receptors subtypes and protein kinase С pathways // J. pharmacol. exp. ther. - 2010. - Vol. 334. - P. 590-598.
13. Paraskevaidis I.A., Parissis J.T., Kremastinos T.D. Antiinflammatory and anti-apoptotic effects of levosimendan in decompensated heart failure: a novel mechanism of drug-induced improvement in contractile performance of the failing heart // Cur. med. chem. cardiovasc. hematol. agents. - 2005. - P. 3 (3). -P. 243-247.
14. Shah V.O., Ferguson J., Hunsaker L.A., Deck L.M., Jagt V. Cardiac glycosides inhibit LPS-induced activation of pro-inflammatory cytokines in whole blood through an NF-kB-dependent mechanism. Int. // J. appl. res. in natural products. - 2011. - Vol. 4 (1). - P. 11-19.
15. Steen M., Kirchberger T., Guse A.H. NAADP mobilizes calcium from the endoplasmic reticular Ca2+ store in T lymphocytes // J. biol. chem. - 2007. - Vol. 282. - P. 18864-18871.
16. Wong M.L., Licino J. Endotoxin-induced myocarditis. Chapter 12. A new Pathophysiological entity in systemic inflammatory response syndrome / Ed. arap Wm Pasqualini R. - CRC Press, 2010. -P. 157-170.
Review
For citations:
Ionov D.I., Fedorova M.M., Sukoyan G.V., Galenko-Yaroshevsky P.A., Gongadze N.V. Efficacy of different cardiotonic drug on severity of endotoxemia under heart failure coupled with systemic inflammatory syndrome in experiments. Kuban Scientific Medical Bulletin. 2015;(6):63-68. (In Russ.)
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