No inducible synthase inhibitors produce a positive effect on indexes of central hemodynamics in rats with septic shock

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The purpose of the study was to evaluate the efficacy of NO inducible synthase (iNOS) inhibitors involved in simulation of septic shock in rats. Model of septic shock (SS) was obtained in rats by intravenous administration of live Bifidobacteria culture. Aminoguanidine was used as a selective inhibitor of iNOS. Indexes of central hemodynamics measured by direct method where analyzed. Vascular endothelial function was rated by determination of nitric oxide (II) (NO), vascular endothelial growth factor A (VEGF-A) and tissue plasminogen activator (tPA) in plasma. Hemostatic parameters were evaluated by the level of soluble fibrin monomer complexes (RKMF). Intravenous administration of live Bifidobacteria culture in rats proved to cause an adequate and effective septic shock model with characteristic changes of hemodynamics in laboratory animals, development of endothelial dysfunction and hemostasis system activation in response to bacteremia. INOS inhibitors have a positive impact on hemodynamics in septic shock. NO is not the only factor in the development of hypotension in septic shock. INOS inhibitors appear to affect the extent of vasopressor dose utilized in the therapy of septic shock contributing to improvement of microcirculation and tissue oxygenation.

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作者简介

Danila Strukov

St. Petersburg State Pediatric Medical University

Email: dstrukov@yandex.ru
Postgraduate Student

Andrey Vasiliev

St. Petersburg State Pediatric Medical University

Email: avas7@mail.ru
MD, PhD, Dr Med Sci, Head, Dept. of Pathophysiology

Yuriy Alexandrovich

St. Petersburg State Pediatric Medical University

Email: jalex1963@mail.ru
MD, PhD, Dr Med Sci, Head, Dept. of Aneasthesiolgic and reanimatologic

参考

  1. Александрович Ю. С., Пшениснов К. В. Современные принципы диагностики и интенсивной терапии септического шока у детей. Российский вестник детской хирургии, анестезиологии и реаниматологии. 2011; 3: 31-6.
  2. Лысикова М., Вальд М., Масиновски З. Механизмы воспалительной реакции и воздействие на них с помощью протеолитических ферментов. Цитокины и воспаление. 2004; 3: 28-34.
  3. Сосунов А. А. Оксид азота как межклеточный посредник. Соросовский образовательный журнал. 2000; 6 (12): 12-8.
  4. Струков Д. В., Васильев А. Г., Александрович Ю. С. Актуальные проблемы сепсиса и септического шока. Педиатр. 2014; 5 (2): 81-7.
  5. Трашков А. П., Васильев А. Г., Дементьева Е. А., Беспалов В. Г., Панченко А. В., Муразов Я. Г. Сравнительная характеристика нарушений работы плазменного компонента системы гемостаза крыс при развитии экспериментальных опухолей различного гистологического типа. Вестник Российской военно-медицинской академии. 2011; 33 (1): 148-53.
  6. Avontuur J. A. M., Bruining H. A., Ince C. Inhibition of Nitric Oxide Synthesis Causes Myocardial Ischemia in Endotoxemic Rats. American Heart Association. 1995; 36: 11-28.
  7. Broderick K. E., Singh V., Zhuang S. et al. Nitric oxide scavenging by the cobalamin precursor cobinamide. J. Biol. Chem. 2005; 8726 (280): 8678-85.
  8. Bruins M. J., Soeters P. B., Lamers Wh. et al. L-arginine supplementation in hyperdynamic endotoxemic pigs: effect on nitric oxide synthesis by the different organs. Crit Care Med. 2002; 30: 508-17.
  9. Dellinger P. R., Mitchell M. L., Andrew R. Surviving Sepsis Campaign. International Guidelines for Management of Severe Sepsis and Septic Shock: Special Article February. 2013; 41 (2): 232-9.
  10. Deutz N. E. P., Hallemeesch M. M., Lamers W. H. et al. The role of iNOS and ecNOS in the in vivo reduction of gut glutamine consumption after endotoxin treatment in mice. FASEB J 6. 2002; 782: 6-22.
  11. Hallemeesch M. M., Soeters P. B., Deutz N. E. P. Renal arginine and protein synthesis are increased during early endotoxemia in mice. Am J Physiol Renal Physiol. 2002; 282: 216-23.
  12. Kent Doi., Asada L., Peter S. T. Star. Animal models of sepsis and sepsis-induced kidney injury. J Clin Invest. 2009; 119 (10): 2868-2878.
  13. Kim H. W., Greenburg A. G. Nitric oxide scavenging, alone or with nitric oxide synthesis inhibition, modulates vascular hyporeactivity in rats with intraperitoneal sepsis. Shock. 2002; 468 (17): 423-6.
  14. Korbut R., Tim D. W., Richard J. G., John R. V. The effect of nitric oxide synthase inhibition on the plasma fibrinolytic system in septic shock in rats. Br. J. Pharmacol. 1994; 112: 289-91.
  15. Mathiak G., Szewczyk D., Abdullah F. An improved clinically relevant sepsis model in the conscious rat. Crit Care Med. 2000; 28 (6): 1947-52.
  16. Price S., Mitchell J. A., Anning P. B. et al. Type II nitric oxide synthase activity is cardio-protective in experimental sepsis. Eur. J. Pharmacol. 2003; 472: 111-8.
  17. Scott J. A., McCormack D. G. Selective in vivo inhibition of inducible nitric oxide synthase in a rat model of sepsis. The American Physiological Society. 1999; 42: 24-32.
  18. Soeters P. B., Hallemeesch M. M., Bruins M. J. Quantitative in vivo assessment of arginine utilization and nitric oxide production in endotoxemia. Am J Surg. 2002; 500 (183): 480-8.
  19. Wink D. A., Miranda K. M., Espey M. G. et al. Mechanisms of the antioxidant effects of nitric oxide. Antioxid Redox Signal. 2001; 236 (3): 203-13.

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