Indicators of cellular metabolism alterationsin patients with traumatic disease due to hypoxia, depending on a management regimen of intensive care
DOI:
https://doi.org/10.14739/2310-1210.2021.6.224373Abstract
The aim of this study was to evaluate changes in the level of erythrocyte metabolism under conditions of hypoxia in patients with traumatic disease in polytrauma depending on the components of intensive care (IC).
Materials and methods. A prospective study was carried out in 88 patients suffering from polytrauma in the period from 2015 to 2017. All the patients were divided into 2 groups, comparable by severity of trauma and condition. A special feature of the examined patients was the staged surgical correction in all cases according to the Damage Control concept.
Patients from the Control group received an intensive care according to the standard local clinical protocol in polytrauma. Patients randomized to the FDP group were treated with infusion of D-fructose-1,6-diphosphate sodium hydrate in addition to the standard care. Hemodynamic parameters and cellular metabolism indicators were monitored: on admission to the operating room, after 24 hours, on day 3, 5 and 14.
Results. The signs of hypovolemia were equally severe in both groups on admission to the operating room. The FDP group demonstrated more rapid stabilization of hemodynamics and improved myocardial contractility at the 3rd day of IC.
The monitoring of acid-base balance and carbohydrate metabolism showed the presence of compensated metabolic acidosis and energy deficiency. High indexes of lactate/pyruvate indicated a sharp imbalance in the ratio of aerobic/anaerobic metabolic processes. The analysis of ATP dynamics displayed impaired mitochondrial ATP production and inhibition of the glycolytic pathway of energy release.
Conclusions. Complementary systemic inflammatory response with the elevation of lactate level by the 5th day occurred in patients with traumatic disease who underwent staged surgical correction. Optimization of intensive care resulted in a faster restoration of the balance between aerobic and anaerobic metabolic processes, an increase in the level of ATP and the rate of 2,3-DPG production in erythrocytes contributing to adequate oxygen supply to the tissues, supporting cellular respiration and preventing the development of oxidative tissue damage, as well as helped to maintain compensatory mechanisms and reduce cellular hypoxia ensuring adequate metabolism of vital organs.
References
Galluzzi, L., Vitale, I., Aaronson, S. A., Abrams, J. M., Adam, D., Agostinis, P., Alnemri, E. S., Altucci, L., Amelio, I., Andrews, D. W., Annicchiarico-Petruzzelli, M., Antonov, A. V., Arama, E., Baehrecke, E. H., Barlev, N. A., Bazan, N. G., Bernassola, F., Bertrand, M., Bianchi, K., Blagosklonny, M. V., … Kroemer, G. (2018). Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018. Cell Death & Differentiation, 25(3), 486-541. https://doi.org/10.1038/s41418-017-0012-4
Bjerkvig, C. K., Strandenes, G., Eliassen, H. S., Spinella, P. C., Fosse, T. K., Cap, A. P., & Ward, K. R. (2016). «Blood failure» time to view blood as an organ: how oxygen debt contributes to blood failure and its implications for remote damage control resuscitation. Transfusion, 56(S2), S182-S189. https://doi.org/10.1111/trf.13500
Ustyantseva, I. M., Khokhlova, O. I., & Kozlov, N. N. (2015). Sindrom sistemnogo vospalitel'nogo otveta i pokazateli gipoksii u patsientov v kriticheskom sostoyanii [Systemic inflammatory response syndrome and hypoxia values in critically ill patients]. Polytrauma, (3), 58-62. [in Russian].
Gaschler, M. M., & Stockwell, B. R. (2017). Lipid peroxidation in cell death. Biochemical and Biophysical Research Communications, 482(3), 419-425. https://doi.org/10.1016/j.bbrc.2016.10.086
Galluzzi, L., Bravo-San Pedro, J. M., Kepp, O., & Kroemer, G. (2016). Regulated cell death and adaptive stress responses. Cellular and Molecular Life Sciences, 73(11-12), 2405-2410. https://doi.org/10.1007/s00018-016-2209-y
Sosin, D. V., Shalaeva, O. E., Yevseyev, A. V., & Shabanov, P. D. (2015). Mekhanizmy formirovaniya ostroi ekzogennoi gipoksii i vozmozhnosti ee farmakologicheskoi korrektsii antigipoksantami [Mechanisms of acute exogenous hypoxia formation and possibilities of its pharmacological correction by antihypoxants]. Obzory po klinicheskoi farmakologii i lekarstvennoi terapii, 13(1), 3-24. https://doi.org/10.17816/RCF1313-24 [in Russian].
Wang, W., Liu, M., You, C., Li, Z., & Zhang, Y. P. (2017). ATP-free biosynthesis of a high-energy phosphate metabolite fructose 1,6-diphosphate by in vitro metabolic engineering. Metabolic Engineering, 42, 168-174. https://doi.org/10.1016/j.ymben.2017.06.006
Lazzarino, G., Nuutinen, M. E., Tavazzi, B., Cerroni, L., Di Pierro, D., & Giardina, B. (1991). Preserving effect of fructose-1,6-bisphosphate on high-energy phosphate compounds during anoxia and reperfusion in isolated langendorff-perfused rat hearts. Journal of Molecular and Cellular Cardiology, 23(1), 13-23. https://doi.org/10.1016/0022-2828(91)90035-k
Sauaia, A., Moore, F. A., & Moore, E. E. (2017). Postinjury Inflammation and Organ Dysfunction. Critical Care Clinics, 33(1), 167-191. https://doi.org/10.1016/j.ccc.2016.08.006
Perlman, R., Callum, J., Laflamme, C., Tien, H., Nascimento, B., Beckett, A., & Alam, A. (2016). A recommended early goal-directed management guideline for the prevention of hypothermia-related transfusion, morbidity, and mortality in severely injured trauma patients. Critical Care, 20(1), Article 107. https://doi.org/10.1186/s13054-016-1271-z
Tsarev, A. V. (2017). Neprednamerennaya gipotermiya i ob"em krovopoteri u patsientov s politravmoi [Intraoperative hypothermia and volume of blood loss of patients with politrauma]. Visnyk problem biolohii i medytsyny, 4(3), 239-242. https://doi.org/10.29254/2077-4214-2017-4-3-141-239-242 [in Russian].
Simmons, J. W., & Powell, M. F. (2016). Acute traumatic coagulopathy: pathophysiology and resuscitation. British Journal of Anaesthesia, 117(Suppl. 3), iii31-iii43. https://doi.org/10.1093/bja/aew328
Baranova, N. V., Lantukhova, N. D., Dolzhenko, M. O., Boyko, O. V., Matveenko, M. S., & Sharlai, K. Yu. (2019). Mozhlyvosti korektsii metabolizmu u patsiientiv z hipoksiieiu zmishanoho henezu pry politravmi (ohliad literatury) [Possibilities of Metabolism Correction in Patients with Hypoxia of Mixed Genesis in Polytrauma (Literature Review)]. Ukrainskyi zhurnal medytsyny, biolohii ta sportu, 4(2), 7-13. https://doi.org/10.26693/jmbs04.02.007 [in Ukrainian].
Alva, N., Alva, R., & Carbonell, T. (2016). Fructose 1,6-Bisphosphate: A Summary of Its Cytoprotective Mechanism. Current Medicinal Chemistry, 23(39), 4396-4417. https://doi.org/10.2174/0929867323666161014144250
Kukes, V. G., Prokofiev, A. B., Checha, O. A., Goroshko, O. A., Mazerkina, I. A., & Demchenkova, E. Yu. (2016). Vliyanie antioksidantov na napryazhenie kisloroda v krovi u patsientov s khronicheskoi serdechnoi nedostatochnost'yu [The effect of antioxidants on oxygen tension in the blood in patients with chronic heart failure]. Mezhdunarodnyi zhurnal prikladnykh i fundamental'nykh issledovanii, (6-1), 56-58. [in Russian].
Marchionni, N., Conti, A., De Alfieri, W., Di Bari, M., Ferrucci, L., Lombardi, A., Moschi, G., Pini, R., & Vannucci, A. (1985). Hemodynamic and electrocardiographic effects of fructose-1,6-diphosphate in acute myocardial infarction. The American Journal of Cardiology, 56(4), 266-269. https://doi.org/10.1016/0002-9149(85)90847-1
Khizhnyak, K. A. (2019). Optymizatsiia anesteziolohichnoho zabezpechennia u khvorykh z khirurhichnym likuvanniam patolohii aorty. (Avtoref. dis. ... kand. med. nauk). [Optimization of anesthetic management in patients with surgical treatment of aortic pathology]. (Extended abstract of candidate’s thesis). Kharkiv. [in Ukrainian].
Kursov, S. V., Nikonov, V. V., & Skoroplit, S. M. (2019). Krovopoterya [Blood loss]. Medytsyna nevidkladnykh staniv, (1), 7-21. https://doi.org/10.22141/2224-0586.1.96.2019.158741 [in Russian].
Kubicek, W. G., Patterson, R. P., & Witsoe, D. A. (1970). IMPEDANCE CARDIOGRAPHY AS A NONINVASIVE METHOD OF MONITORING CARDIAC FUNCTION AND OTHER PARAMETERS OF THE CARDIOVASCULAR SYSTEM. Annals of the New York Academy of Sciences, 170(2), 724-732. https://doi.org/10.1111/j.1749-6632.1970.tb17735.x
Kamyshnikov, V.S. (Ed.). (2016). Metody klinicheskikh laboratornykh issledovanii [Methods of clinical and laboratory examinations] (8th ed.). MEDpress-inform. [in Russian].
Vinogradova, I. L., Bagryantseva, S. Yu., & Derviz, G. V. (1980). Metod odnovremennogo opredeleniya 2,3-DFG i ATF v eritrotsitakh [A method of simultaneous determination of 2,3-DPG and ATP in erythrocytes]. Laboratornoe delo, (7), 424-426. [in Russian].
Cecconi, M., De Backer, D., Antonelli, M., Beale, R., Bakker, J., Hofer, C., Jaeschke, R., Mebazaa, A., Pinsky, M. R., Teboul, J. L., Vincent, J. L., & Rhodes, A. (2014). Consensus on circulatory shock and hemodynamic monitoring. Task force of the European Society of Intensive Care Medicine. Intensive Care Medicine, 40(12), 1795-1815. https://doi.org/10.1007/s00134-014-3525-z
Lebedinskii, K. M. (Ed.). (2012). Krovoobrashchenie i anesteziya. Otsenka i korrektsiya sistemnoi gemodinamiki vo vremya operatsii i anestezii [Circulation and Anaesthesia. Systemic circulation assessment and management during surgery and anaesthesia]. Chelovek. [in Russian].
Vincent, J. L., Quintairos E Silva, A., Couto, L., Jr, & Taccone, F. S. (2016). The value of blood lactate kinetics in critically ill patients: a systematic review. Critical Care, 20(1), Article 257. https://doi.org/10.1186/s13054-016-1403-5
Patet, C., Suys, T., Carteron, L., & Oddo, M. (2016). Cerebral Lactate Metabolism After Traumatic Brain Injury. Current Neurology and Neuroscience Reports, 16(4), Article 31. https://doi.org/10.1007/s11910-016-0638-5
Singer, M., Deutschman, C. S., Seymour, C. W., Shankar-Hari, M., Annane, D., Bauer, M., Bellomo, R., Bernard, G. R., Chiche, J. D., Coopersmith, C. M., Hotchkiss, R. S., Levy, M. M., Marshall, J. C., Martin, G. S., Opal, S. M., Rubenfeld, G. D., van der Poll, T., Vincent, J. L., & Angus, D. C. (2016). The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA, 315(8), 801-810. https://doi.org/10.1001/jama.2016.0287
Li, T. T., Xie, J. Z., Wang, L., Gao, Y. Y., & Jiang, X. H. (2015). Rational application of fructose-1,6-diphosphate: From the perspective of pharmacokinetics. Acta Pharmaceutica, 65(2), 147-157. https://doi.org/10.1515/acph-2015-0020
Antunes, N., Martinusso, C. A., Takiya, C. M., da Silva, A. J., de Ornellas, J. F., Elias, P. R., Leite, M., Jr, & Cardoso, L. R. (2006). Fructose-1,6 diphosphate as a protective agent for experimental ischemic acute renal failure. Kidney international, 69(1), 68-72. https://doi.org/10.1038/sj.ki.5000013
Gawarammana, I., Mohamed, F., Bowe, S. J., Rathnathilake, A., Narangoda, S. K., Azher, S., Dawson, A. H., & Buckley, N. A. (2010). Fructose-1, 6-diphosphate (FDP) as a novel antidote for yellow oleander-induced cardiac toxicity: a randomized controlled double blind study. BMC Emergency Medicine, 10, Article 15. https://doi.org/10.1186/1471-227X-10-15
Kalam, Y., & Graudins, A. (2012). The effects of fructose-1,6-diphosphate on haemodynamic parameters and survival in a rodent model of propranolol and verapamil poisoning. Clinical Toxicology, 50(7), 546-554. https://doi.org/10.3109/15563650.2012.705847
Tikhonova, L. A. (2017). Toksicheskoe deistvie beta-amiloidnogo peptida 25-35 na eritrotsity raznykh vozrastnykh populyatsii. (Avtoref. dis. ... kand. biol. nauk). [Toxic effect of amyloid-beta (25-35) peptide on erythrocytes of different age populations]. (Extended abstract of candidate’s thesis). Pushchino. [in Russiаn].
Downloads
Published
How to Cite
Issue
Section
License
Authors who publish with this journal agree to the following terms:- Authors retain copyright and grant the journal right of first publication with the work simultaneously licensed under a Creative Commons Attribution License that allows others to share the work with an acknowledgement of the work's authorship and initial publication in this journal.
- Authors are able to enter into separate, additional contractual arrangements for the non-exclusive distribution of the journal's published version of the work (e.g., post it to an institutional repository or publish it in a book), with an acknowledgement of its initial publication in this journal.
- Authors are permitted and encouraged to post their work online (e.g., in institutional repositories or on their website) prior to and during the submission process, as it can lead to productive exchanges, as well as earlier and greater citation of published work (See The Effect of Open Access)
