Dynamics of serum levels of nitrogen oxide and hydrogen sulfide metabolites as markers of organ dysfunction in acute phase of multiple trauma
Background. Patients with multiple organ and system traumas are at high risk of shock, complications and death during few years of follow-up. Nowadays, all known scales used to determine the severity of multiple trauma and its prognosis are of limited sensitivity because of their subjectivity. In recent years, a lot of attention is paid to gas transmitters, in particular nitrogen oxide (NO), carbon monoxide (СО) and hydrogen sulfide (H2S). Since the tissue damage results in the elevation of gas transmitter production by different cells it can be assumed that the levels of gas transmitters and oxidized products in the blood serum serve as markers of multiple trauma and correlates with its prognosis. This investigation was done to determine the severity of endothelial dysfunction and the role of gas transmitters as markers of organ dysfunction in acute phase of multiple trauma. Materials and methods. Clinical study and treatment data of 28 multiple trauma patients are presented. The mean age of them was 48.4 ± 5.2 years. Upon admission, all patients were stratified according to Acute Physiology and Chronic Health Evaluation II scale depending on trauma severity: group 1 (n = 22) — with moderate and group 2 (n = 6) — with severe multiple trauma. Results. The significant decrease of NO concentration occurred in both groups already at the admission as compared to the normal values (0.49 ± 0.06 μmol/l, р = 0.001). The concentration of NO in the blood serum increased to 0.43 ± 0.03 μmol/l and 0.45 ± 0.03 μmol/l, respectively, after 24 hours in the intensive care unit. At admission, the difference between the mean levels of NOx in the blood serum of patients from two groups was significant (р = 0.003). Intensive therapy resulted in the increase of NO2 + NO3 concentration in both groups (р = 0.001 compared to the baseline), and the difference between groups was not statistically significant anymore (р = 0.475). Upon admission, the mean level of H2S in the blood serum of patients from both groups was significantly higher than normal (р = 0.025). The difference between groups was not significant (р = 0.117). Intensive care was accompanied by the normalization of H2S level. Conclusions. The endothelial dysfunction occurs in patients with acute multiple trauma which is confirmed by significant changes of gas transmitter levels in the blood serum. The concentrations of NO and its oxidized products (NOx) at admission serve as the sensible markers of multiple trauma severity. The low level of NOx upon admission in patients with extremely severe trauma can predict an unfavourable outcome of the acute phase of multiple trauma.
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Berezovs'kij VJa, Plotnіkova LM. The role of endogenous hydrogen sulfide in the regulation of physiological functions of the organism. Medical hydrology and rehabilitation. 2013;1:117–122. (In Ukrainian).
Nasibullin BA, Gozhenko A.I. The cycle of nitric oxide and the activity of the central nervous system. Patologіja.2005;2(3):1519. (In Ukrainian).
Shliakhto EV, Berkovich OA, Beliaeva LB. Modern concepts of endothelial dysfunction and methods of its correction in atherosclerosis. International neurological Journal. 2002;3:9-13. (in Russian).
Daiber A, Steven S, Weber A, et al. Targeting vascular (endothelial) dysfunction. Br. J. Pharmacol. 2016; doi: 10.1111/bph.13517.
Moreira JD, Pernomia NL, Gomes MS et al. Enhanced nitric oxide generation from nitric oxide synthases as the cause of increased peroxynitrite formation during acute restraint stress: Effects on carotid responsiveness to angiotensinergic stimuli in type-1 diabetic rats. Eur. J. Pharmacol. 2016;783:11-22. doi: 10.1016/j.ejphar.2016.04.050. Epub 2016 Apr 23.
Novickij VV, Rjazanceva NV, Starikova EG et al. Regulation of cell apoptosis using gas transducers (nitrogen oxide, carbon monoxide and hydrogen sulfide). Herald of Science in Siberia. 2011;1:635-640.
Hsieh HJ, Liu CA, Huang B, Tseng AH, Wang DL. Shear-induced endothelial mechanotransduction: the interplay between reactive oxygen species (ROS) and nitric oxide (NO) and the pathophysiological implications. J. Biomed. Sci. 2014;21:3. doi: 10.1186/1423-0127-21-3.
Zhao W, Zhang J, Lu Y, Wang R. The vasorelaxant effect of H2S as a novel endogenous gaseous KATP channel opener. EMBO J. 2001;20:6008–6016. doi:10.1093/emboj/20.21.6008.
Chen X., Jhee K.H., Kruger W.D. Production of the neuromodulator H2S by cystathionine beta-synthase via the condensation of cysteine and homocysteine. J. Biol. Chem. 2004;279:52082–52086. DOI: 10.1074/jbc.C400481200.
Cacanyiova S., Berenyiova A., Kristek F. The Role of Hydrogen Sulphide in Blood Pressure Regulation. Physiol. Res. 2016;65:273-289. PMID: 27775417.
Mjasoedova OA, Korzhov VI. The role of hydrogen sulfide in the implementation of the physiological functions of the body. Zhurnal NAMN Ukrainy. 2011;17(3):191-199. (In Ukrainian).
Said MA, El-Gohary OA. Effect of noise stress on cardiovascular system in adult male albino rat: implication of stress hormones, endothelial dysfunction and oxidative stress. Gen. Physiol. Biophys. 2016;35:371-377. doi: 10.4149/gpb_2016003. Epub 2016 May 13.
Sakemi K, Ohno Y, Tsuda M. NO2-/NO3- levels in blood and principal organs in rats treated with lipopolysaccharide. Kokuritsu Iyakuhin Shokuhin Eisei Kenkyusho Hokoku. 1998;116:101-106.
Chapleau W, Al-khatib J, Haskin D, et al. Advanced trauma life support (ATLS®): the ninth edition. ATLS Subcommittee; American College of Surgeons’ Committee on Trauma; International ATLS working group. J. Trauma Acute Care Surg. 2013; 74(5): 1363-1366. doi: 10.1097/TA.0b013e31828b82f5.
Malyshev IY. Manukhina EB. Stress, adaptation, and nitric oxide. Biochemistry. Moscow. 1998;63:840-853. (in Russian).
Song Y, Wang L. Hydrogen sulfide and acute lung injury.World Journal of Pharmacy and Pharmaceutical Sciences. 2016;5:367-386. DOI: 10.20959/wjpps201612-7760.
Beitl E., Banasova A., Vlcek M., Mikova D., Hampl V. Nitric oxide as an indicator for severity of injury in polytrauma. Bratislava Medical Journal. 2016;116, :217-220. PMID: 27075385.
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