Эффективность Реамберина в программе лечения острого панкреатита тяжелой степени
Эффективность Реамберина в программе лечения острого панкреатита тяжелой степени
Орлов Ю.П., Говорова Н.В., Глущенко А.В. и др. Эффективность Реамберина в программе лечения острого панкреатита тяжелой степени. Гастроэнтерология. Хирургия. Интенсивная терапия. Consilium Medicum. 2019; 2: 24–27. DOI: 10.26442/26583739.2019.2.190389
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Orlov Yu.P., Govorova N.V., Glushchenko A.V. et al. Efficiency of Reamberin in the program of treatment of acute pancreatitis heavy degree. Gastroenterology. Surgery. Intensive care. Consilium Medicum. 2019; 2: 24–27. DOI: 10.26442/26583739.2019.2.190389
Эффективность Реамберина в программе лечения острого панкреатита тяжелой степени
Орлов Ю.П., Говорова Н.В., Глущенко А.В. и др. Эффективность Реамберина в программе лечения острого панкреатита тяжелой степени. Гастроэнтерология. Хирургия. Интенсивная терапия. Consilium Medicum. 2019; 2: 24–27. DOI: 10.26442/26583739.2019.2.190389
________________________________________________
Orlov Yu.P., Govorova N.V., Glushchenko A.V. et al. Efficiency of Reamberin in the program of treatment of acute pancreatitis heavy degree. Gastroenterology. Surgery. Intensive care. Consilium Medicum. 2019; 2: 24–27. DOI: 10.26442/26583739.2019.2.190389
Острый панкреатит остается актуальной проблемой не только для хирургии, но и для реаниматологии. Тяжесть острого панкреатита, независимо от этиологического фактора, в общем аспекте обусловлена гипоксическим компонентом на уровне панкреатоцита, что является следствием расстройств микроциркуляции на фоне воспаления, активации свободно-радикального окисления и митохондриальной дисфункции. Использование у пациентов в программе интенсивной патогенетически обоснованной терапии препаратов, содержащих янтарную кислоту, как раз и решает проблему на уровне митохондрий. Это позволяет достичь не только положительной динамики со стороны электролитов плазмы крови, восстановления реологических ее параметров, но и эффективной динамики снижения уровня активности ферментов (как в крови, так и в моче) и уровня воспалительного компонента, что косвенно является следствием восстановления микроциркуляции, устранения эффектов гипоксии на уровне митохондрий в структуре железы.
Acute pancreatitis remains a burning issue not only for surgery, but also for resuscitation. The severity of acute pancreatitis, regardless of etiological factor in the overall aspect of the due gipoksicheskim pankreatocita-level component that is a consequence of disorders of microcirculation amid inflammation, activation of free radical oxidation and mitochondrial dysfunction. Use in patients in the intensive programme, pathogenetically therapy, drugs that contain amber acid, solves the problem at the level of the mitochondria. This allows you to achieve positive dynamics, not only by blood plasma electrolytes, restore its rheological parameters, but also effective dynamics of declining levels of enzyme activity, as in the blood and in the urine and the level of inflammatory component, which indirectly is the result of restoration of microcirculation, eliminating the effects of hypoxia on mitochondria in the level structure of the gland.
1. Papachristou GI. Prediction of severe acute pancreatitis: current knowledge and novel insights. World J Gastroenterol 2008; 14: 6273–5.
2. Zhang H, Neuhöfer P, Song L et al. IL-6 trans-signaling promotes pancreatitis-associated lung injury and lethality. J Clin Invest 2013; 123: 1019–31.
3. Carrasco C, Rodriguez AB, Pariente JA. Effects of melatonin on the oxidative damage and pancreatic antioxidant defenses in cerulein-induced acute pancreatitis in rats. Hepatobiliary Pancreatic Dis Int 2014; 13 (4): 442–6.
4. Park BK, Chung JB, Lee JH et al. Role of oxygen free radicals in patients with acute pancreatitis. World J Gastroenterol 2003; 9 (10): 2266–9.
5. Maciejczyk M, Skutnik-Radziszewska A, Zieniewska I et al. Antioxidant Defense, Oxidative Modification. Functioninan Early Phase of Cerulein Pancreatitis. Oxid Med Cell Longev 2019; 2019: 8403578.
6. Halliwell B, Gutteridge JM, Cross CE. Free radicals, antioxidants, and human disease: Where are we now? J Lab Clin Med 1992; 119: 598–620.
7. Lukyanova LD. Current issues of adaptation to hypoxia. Signal mechanisms and their role in system regulation. Patol Fiziologiia Eksperim Terapiia 2011; 1: 3–19.
8. Chance B, Williams GR. A method for the localization of sites for oxidative phosphorylation. Nature 1955; 176 (4475): 250–4.
9. Chance B, Williams GR. Respiratory enzymes in oxidative phosphorylation. VI. The effects of adenosine diphosphate on azide-treated mitochondria. J Biol Chem 1956; 221 (1): 477–89.
10. Ranson JH et al. Prognostic signs and the role of operativemanagement in acute pancreatitis. Surg Gynecol Obstet 1974; 139 (1): 69–81.
11. Singer M, Deuschman CS, Seymour CW et al. The Third International Consensus definitions for Sepsis and Septic Shock (Sepsis-3). JAMA 2016; 315 (8): 801–10.
12. Toouli J, Brooke-Smith M, Bassi C et al. Guidelines for the management of acute pancreatitis. J Gastroenterol Hepatol 2002; 17: 15–39.
13. Peti-Peterdi J, Kishore BK, Pluznick JL et al. Regulation of Vascular and Renal Function by Metabolite Receptors. Annu Rev Physiol 2016; 78: 391–414.
14. He W, Miao FJ, Lin DC. Citric acid cycle intermediates as ligands for orphan G-protein-coupled receptors. Nature 2004; 429 (6988): 188–93.
15. Krebs HA. Rate control of the tricarboxylic acid cycle. Adv Enzyme Regul 1970; 8: 335–53.
16. Pell VR, Chouchani ET, Frezza C et al. Succinate metabolism: a new therapeutic target for myocardial reperfusion injury. Cardiovasc Res 2016; 111 (2): 134–41.
17. Hawkins BJ, Levin MD, Doonan PJ et al. Mitochondrial complex II prevents hypoxic but not calcium- and proapoptotic Bcl-2 protein-induced mitochondrial membrane potential loss. J Biol Chem 2010; 285 (34): 26494–505.
18. Zhang J, Wang YT, Miller JH et al. Accumulation of Succinate in Cardiac Ischemia Primarily Occurs via Canonical Krebs Cycle Activity. Cell Rep 2018; 23 (9): 2617–28.
________________________________________________
1. Papachristou GI. Prediction of severe acute pancreatitis: current knowledge and novel insights. World J Gastroenterol 2008; 14: 6273–5.
2. Zhang H, Neuhöfer P, Song L et al. IL-6 trans-signaling promotes pancreatitis-associated lung injury and lethality. J Clin Invest 2013; 123: 1019–31.
3. Carrasco C, Rodriguez AB, Pariente JA. Effects of melatonin on the oxidative damage and pancreatic antioxidant defenses in cerulein-induced acute pancreatitis in rats. Hepatobiliary Pancreatic Dis Int 2014; 13 (4): 442–6.
4. Park BK, Chung JB, Lee JH et al. Role of oxygen free radicals in patients with acute pancreatitis. World J Gastroenterol 2003; 9 (10): 2266–9.
5. Maciejczyk M, Skutnik-Radziszewska A, Zieniewska I et al. Antioxidant Defense, Oxidative Modification. Functioninan Early Phase of Cerulein Pancreatitis. Oxid Med Cell Longev 2019; 2019: 8403578.
6. Halliwell B, Gutteridge JM, Cross CE. Free radicals, antioxidants, and human disease: Where are we now? J Lab Clin Med 1992; 119: 598–620.
7. Lukyanova LD. Current issues of adaptation to hypoxia. Signal mechanisms and their role in system regulation. Patol Fiziologiia Eksperim Terapiia 2011; 1: 3–19.
8. Chance B, Williams GR. A method for the localization of sites for oxidative phosphorylation. Nature 1955; 176 (4475): 250–4.
9. Chance B, Williams GR. Respiratory enzymes in oxidative phosphorylation. VI. The effects of adenosine diphosphate on azide-treated mitochondria. J Biol Chem 1956; 221 (1): 477–89.
10. Ranson JH et al. Prognostic signs and the role of operativemanagement in acute pancreatitis. Surg Gynecol Obstet 1974; 139 (1): 69–81.
11. Singer M, Deuschman CS, Seymour CW et al. The Third International Consensus definitions for Sepsis and Septic Shock (Sepsis-3). JAMA 2016; 315 (8): 801–10.
12. Toouli J, Brooke-Smith M, Bassi C et al. Guidelines for the management of acute pancreatitis. J Gastroenterol Hepatol 2002; 17: 15–39.
13. Peti-Peterdi J, Kishore BK, Pluznick JL et al. Regulation of Vascular and Renal Function by Metabolite Receptors. Annu Rev Physiol 2016; 78: 391–414.
14. He W, Miao FJ, Lin DC. Citric acid cycle intermediates as ligands for orphan G-protein-coupled receptors. Nature 2004; 429 (6988): 188–93.
15. Krebs HA. Rate control of the tricarboxylic acid cycle. Adv Enzyme Regul 1970; 8: 335–53.
16. Pell VR, Chouchani ET, Frezza C et al. Succinate metabolism: a new therapeutic target for myocardial reperfusion injury. Cardiovasc Res 2016; 111 (2): 134–41.
17. Hawkins BJ, Levin MD, Doonan PJ et al. Mitochondrial complex II prevents hypoxic but not calcium- and proapoptotic Bcl-2 protein-induced mitochondrial membrane potential loss. J Biol Chem 2010; 285 (34): 26494–505.
18. Zhang J, Wang YT, Miller JH et al. Accumulation of Succinate in Cardiac Ischemia Primarily Occurs via Canonical Krebs Cycle Activity. Cell Rep 2018; 23 (9): 2617–28.