Efekti hiperbarične oksigenacije na kardiodinamiku i oksidacioni stres kod pacova sa sepsom

  • Aleksandar Jevtić Institute for Orthopedic Surgery “Banjica”, Belgrade, Serbia
  • Vladimir Živković University of Kragujevac, Faculty of Medical Sciences, Department of Physiology, Kragujevac, Serbia
  • Milica Milinković University of Kragujevac, Faculty of Medical Sciences, Department of Physiology, Kragujevac, Serbia
  • Željko Mijailović University of Kragujevac, Faculty of Medical Sciences, Department of Pharmacy, Kragujevac, Serbia
  • Nevena Draginić University of Kragujevac, Faculty of Medical Sciences, Department of Pharmacy, Kragujevac, Serbia
  • Marijana Andjić University of Kragujevac, Faculty of Medical Sciences, Department of Pharmacy, Kragujevac, Serbia
  • Andjela Milojević Šamanović Department of Dentistry, Faculty of Medical Sciences, University of Kragujevac, Kragujevac, Serbia
  • Sergey Bolevich 1st Moscow State Medical University IM Sechenov, Department of Human Pathology, Moscow, Russian Federation
  • Vladimir Jakovljević University of Kragujevac, Faculty of Medical Sciences, Department of Physiology, Kragujevac, Serbia
Ključne reči: hiperbarička oksigenacija, stres, oksidativni, sepsa, srce, pacovi

Sažetak


Uvod/Cilj. Disfunkcija na nivou ćelije, tkiva ili organa, koja može imati za posledicu smrtni ishod, javlja se usled metaboličkih promena i poremećaja regulacije transkripcije gena i mikro- i makro cirkulacije. Cilj ove studije bio je da se proceni uticaj hiperbarične oksigenacije (HBO) na izolovano srce, kao i na oksidacioni status pacova sa sepsom. Metode. Istraživanjem su obuhvaćeni mužjaci Wistar albino pacova klasifikovani u tri grupe: prva grupa je bila kontrolna grupa (CTRL), drugu grupu su činile životinje izložene samo sepsi bez HBO tretmana (grupa Sepsa), dok su u trećoj grupi životinje tretirane HBO nakon indukcije sepse (grupa Sepsa + HBO). Za indukciju sepse korišćen je model fekalnog peritonitisa (3 mL/kg fekalne suspenzije, intraperitonealno). Posle indukcije sepse, pacovi su bili izloženi dva puta dnevno (tokom 12 sati) HBO tretmanu sa 2,8 apsolutnih atmosfera (ATA) tokom 90 minuta u periodu od 3 dana. 72 h nakon potvrđivanja sepse, životinje su žrtvovane, a srca su retrogradno perfundovana na Langendorfovom aparatu, pri postepenom povećanju koronarnog perfuzionog pritiska (CPP = 40–120 cm H2O). Sledeći parametri srčane funkcije su kontinuirano mereni: maksimalna i minimalna stopa promene pritiska u levoj komori (dp/dt max, dp/dt min); sistolni i dijastolni pritisak leve komore (SLVP i DLVP) i srčana frekvenca (HR). Koronarni protok (CF) je meren floumetrijski. Određivani su sledeći markeri oksidacionog stresa: nitriti (NO2), superoksid anjon radikal (O2), vodonik peroksid (H2O2), indeks lipidne peroksidacije (TBARS), aktivnost superoksid dismutaze (SOD) i katalaze (CAT) i nivo redukovanog glutationa (GSH). Rezultati. Nije bilo značajne razlike u dp/dt max, dp/dt min, SLVP i HR između grupa. CF je bio statistički značajno veći (p < 0,01) u grupi sa sepsom. Vrednosti svih srčanih oksidacionih markera bile su niže u grupi sepsa + HBO (p < 0,05), dok su sistemski pro-oksidacioni i antioksidacioni parametri bili nepromenjeni. Zaključak. Naši rezultati su pokazali da HBO tretman nije bio povezan sa poboljšanom funkcijom srca i koronarnom perfuzijom, dok je ostvario obećavajući korisne efekte na oksidacioni status u srcu pacova.

Biografija autora

Vladimir Živković, University of Kragujevac, Faculty of Medical Sciences, Department of Physiology, Kragujevac, Serbia

 

 

Reference

Gyawali B, Ramakrishna K, Dhamoon AS. Sepsis: The evolution in definition, pathophysiology, and management. SAGE Open Med 2019; 7: 2050312119835043.

Manfredini A, Constantino L, Pinto MC, Michels M, Burger H, Kist LW, еt al. Mitochondrial dysfunction is associated with long-term cognitive impairment in an animal sepsis model. Clin Sci (Lond) 2019; 133(18): 1993–2004.

Rello J, Valenzuela-Sánchez F, Ruiz-Rodriguez M, Moyano S. Sep-sis: A review of advances in management. Adv Ther 2017; 34(11): 2393–411.

Fattahi F, Ward PA. Complement and sepsis-induced heart dysfunction. Mol Immunol 2017; 84: 57–64.

Gupta A, Brahmbhatt S, Kapoor R, Loken L, Sharma AC. Chron-ic peritoneal sepsis: myocardial dysfunction, endothelin and signaling mechanisms. Front Biosci 2005; 10: 3183–205.

Chopra M, Sharma AC. Distinct cardiodynamic and molecular characteristics during early and late stages of sepsis-induced myocardial dysfunction. Life Sci 2007; 81(4): 306–16.

Chopra M, Sharma AC. Apoptotic cardiomyocyte hypertrophy during sepsis and septic shock results from prolonged exposure to endothelin precursor. Front Biosci 2007; 12: 3052–60.

Babul S, Rhodes EC. The role of hyperbaric oxygen therapy in sports medicine. Sports Med 2000; 30(6): 395–403.

Poff AM, Kernagis D, D'Agostino DP. Hyperbaric environment: oxygen and cellular damage versus protection. Compr Physiol 2016; 7(1): 213–34.

Bennett M, Best TM, Babul S, Taunton J, Lepawsky M. Hyperbar-ic oxygen therapy for delayed onset muscle soreness and closed soft tissue injury. Cochrane Database Syst Rev 2005; (4): CD004713.

Demchenko IT, Zhilyaev SY, Moskvin AN, Krivchenko AI, Pian-tadosi CA, Allen BW. Baroreflex-mediated cardiovascular re-sponses to hyperbaric oxygen. J Appl Physiol 2013; 115(6): 819–28.

Bergo GW, Tyssebotn I. Cardiovascular effects of hyperbaric oxygen with and without addition of carbon dioxide. Eur J Appl Physiol Occup Physiol 1999; 80(4): 264–75.

Halbach JL, Prieto JM, Wang AW. Early hyperbaric oxygen therapy improves survival in a model of severe sepsis. Am J Physiol Regul Integr Comp Physiol 2019; 317(1): R160–8.

Tai PA, Chang CK, Niu KC, Lin MT, Chiu WT, Lin JW. Re-duction of ischemic and oxidative damage to the hypothala-mus by hyperbaric oxygen in heatstroke mice. J Biomed Bio-technol 2010; 2010: 609526.

Zolfaghari PS, Pinto BB, Dyson A, Singer M. The metabolic phe-notype of rodent sepsis: cause for concern? Intensive Care Med Exp 2013; 1(1): 25.

Ozturk А, Yamanel L, Ozenc S, Ince M, Simsek K, Comert B, et al. Comparison of the effects of hyperbaric oxygen and nor-mobaric oxygen on sepsis in rats. Arch Clin Exp Surg 2016; 5(1): 7–12.

Green LC, Wagner DA, Glogowski J, Skipper PL, Wishnok JS, Tannenbaum SR. Analysis of nitrate, nitrite, and [15N] nitrate in biological fluids. Anal Biochem 1982; 126(1): 131–8.

Pick E, Keisari Y. A simple colorimetric method for the meas-urement of hydrogen peroxide produced by cells in culture. J Immunol Methods 1980; 38(1‒2): 161–70.

Ohkawa H, Ohishi N, Yagi K. Assay for lipid peroxides in ani-mal tissues by thiobarbituric acid reaction. Anal Biochem 1979; 95(2): 351–8.

Auclair C, Voisin E. Nitroblue tetrazolium reduction. In: Greenvvald RA, editor. Handbook of methods for oxygen radi-cal research. Boca Raton: CRC Press; 1985. p. 123–32.

McCord JM, Fridovich I. The utility of superoxide dismutase in studying free radical reactions. I. Radicals generated by the in-teraction of sulfite, dimethyl sulfoxide, and oxygen. J Biol Chem 1969; 244(22): 6056–63.

Misra HP, Fridovich I. The role of superoxide-anion in the au-tooxidation of epinephrine and a simple assay for superoxide dismutase. J Biol Chem 1972; 247(10): 3170–5.

Beutler E. Catalase. In: Beutler E editor. Red cell metabolism, a manual of biochemical methods. New York, NY, USA: Grune and Stratton; 1982. p. 105–6.

Beutler E. Reduced glutathione (GSH). In: Beutler E editor. Red cell metabolism, a manual of biochemical methods. New York, NY, USA: Grune and Stratton; 1975. p. 112–4.

Zhai X, Yang Z, Zheng G, Yu T, Wang P, Liu X, et al. Lactate as a potential biomarker of sepsis in a rat cecal ligation and puncture model. Mediators Inflamm 2018; 2018: 8352727.

Drosatos K, Lymperopoulos A, Kennel PJ, Pollak N, Schulze PC, Goldberg IJ. Pathophysiology of sepsis-related cardiac dysfunc-tion: driven by inflammation, energy mismanagement, or both? Curr Heart Fail Rep 2015; 12(2): 130–40.

de Montmollin E, Aboab J, Mansart A, Annane D. Bench-to-bedside review: beta-adrenergic modulation in sepsis. Crit Care 2009; 13(5): 230.

Drosatos K, Khan RS, Trent CM, Jiang H, Son NH, Blaner WS, et al. Peroxisome proliferator-activated receptor-γ activation prevents sepsis-related cardiac dysfunction and mortality in mice. Circ Heart Fail 2013; 6(3): 550–62.

Yang ZJ, Bosco G, Montante A, Ou XI, Camporesi EM. Hyper-baric O2 reduces intestinal ischemia-reperfusion-induced TNF-alpha production and lung neutrophil sequestration. Eur J Appl Physiol 2001; 85(1‒2): 96–103.

Chang KY, Tsai PS, Huang TY, Wang TY, Yang S, Huang CJ. HO-1 mediates the effects of HBO pretreatment against sep-sis. J Surg Res 2006; 136(1): 143–53.

Rudiger A, Dyson A, Felsmann K, Carré JE, Taylor V, Hughes S, et al. Early functional and transcriptomic changes in the myo-cardium predict outcome in a long-term rat model of sepsis. Clin Sci (Lond) 2013; 124(6): 391–401.

Lin HC, Wan FJ, Wu CC, Tung CS, Wu TH. Hyperbaric oxy-gen protects against lipopolysaccharide-stimulated oxidative stress and mortality in rats. Eur J Pharmacol 2005; 508(1‒3): 249–54.

Edremitlioğlu M, Kiliç D, Oter S, Kisa U, Korkmaz A, Coşkun O, et al. The effect of hyperbaric oxygen treatment on the renal functions in septic rats: relation to oxidative damage. Surg Today 2005; 35(8): 653–61.

Oter S, Edremitlioglu M, Korkmaz A, Coskun O, Kilic D, Kisa U, et al. Effects of hyperbaric oxygen treatment on liver func-tions, oxidative status and histology in septic rats. Intensive Care Med 2005; 31(9): 1262–8.

Bektas A, Ulusoy M, Mas MR. Do late phase hyperbaric and normobaric oxygen therapies have effect on liver damage? An experimental sepsis model. Gen Med (Los Angel) 2019; 7(1): 324.

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2021/08/24
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