Role of gaseous transmitters in the pathogenesis of organ dysfunction in multiple trauma

N.V. Matolinets

Abstract


The review of modern data about the role of gaseous transmitters in multiple trauma patients with regard to the theory of stress and pathogenesis of major complications is presented. It is known that the system of nitric oxide (NO) production is the stress-limiting system. Mechanisms responsible for the development of stress-induced reactions include both the increase of sympathetic nervous system activity, glucocorticoid overload that correlates with severity of clinical symptoms, and the change of endothelial function, including the reduction of NO bioavailability. Oxidative stress is an important determinant of endothelial dysfunction development. The reactive oxygen species also change hydrogen sulfide-related mechanisms, which influence the signaling pathways of endothelium. The hydrogen sulfide (H2S) has a unique mechanism of action on vessels, protects neurons from oxidative stress. NО also acts as an antioxidant that inhibits free-radical reactions in physiological conditions. There are reports about cross reactions between H2S and NO that form a nitrosothiol complex, which acts as a new way of signal transmission and is an important factor of forming protective and pathological reactions to the action of acute stress factors. Currently, an active search is being conducted for effective prognosticators of multiple trauma outcomes and means to correct secondary organ damage (cerebrum, lungs, kidneys) that can result in multiple organ failure. The dependence of NO production on trauma severity, as well as its multimodal impact on complications pathogenesis in relation to the stress reaction allows considering it as prognostic marker of multiple trauma outcome. The use of active gaseous transmitter precursors (L-arginine as NO donator, sodium hydrosulfide as H2S donator) allows elaborating new treatment modalities for critically ill patients with multiple injuries, although the mechanisms of their action and interactions need further research.

Keywords


multiple trauma; multiple organ failure; gaseous transmitters; nitric oxide; hydrogen sulfide; review

References


Injuries and violence: the facts 2014. World Health Organization. Available from: http://apps.who.int/iris/bitstream/10665/149798/1/9789241508018_eng.pdf. Accessed: 2014

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.

R.F. Shere-Wolfe, S.M. Galvagno, T.E. Grissom. Critical care considerations in the management of the trauma patient following initial resuscitation. Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine. 2012;20:68. doi: 10.1186/1757-7241-20-68.

Kharkevych N.H. Clinico-pathogenetic features of closed craniocerebral trauma in the aspect of stressа [Kliniko-patogeneticheskie osobennosti zakrytoi cherepno-mozgovoi travmy v aspekte stressa ] Moscow: 1983. 35 p. (in Russian).

Nickel T, Deutschmann A, Hanssen H, et al. Modification of endothelial biology by acute and chronic stress hormones. Microvasc. Res. 2009; 78:364-369.

Goodwin JE, Geller DS. Glucocorticoid-induced hypertension. Pediatr. Nephrol. 2012; 27:1059-1066. doi: 10.1016/j.mvr.2009.07.008.

Strawn WB, Bondjers G, Kaplan JR. Endothelial dysfunction in response to psychosocial stress in monkeys. Circ. Res. 1991;68:1270-1279.

Skantze HB, Kaplan J, Pettersson K, et al. Psychosocial stress causes endothelial injury in cynomolgus monkeys via beta1-adrenoceptor activation. Atherosclerosis. 1998;136:153-161.

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.

Sriram K, Laughlin JG, Rangamani P, Tartakovsky DM. Shear-induced nitric oxide production by endothelial cells. Biophys. J. 2016;111:208-221. doi: 10.1016/j.bpj.2016.05.034.

Sivonová M, Zitnanová I, Hlincíková L, Skodácek I, Trebatická J, Duracková Z. Oxidative stress in university students during examinations. Stress. 2004;7:183-188.

Malyshev IY. Manukhina EB. Stress, adaptation, and nitric oxide. Biochemistry. Moscow. 1998;63:840-853.

Parshina S. S. Modern ideas about the biological effects of nitric oxide and its role in the development of cardiovascular patholog. Cardiovascular therapy and prevention. 2006;1:88-94. (in Russian).

Zozulia Iu. A., Sen'ko L. N. Cerebral vasospasm after subarachnoid hemorrhage. Molecular aspects of endothelial dysfunction. Ukrainian Journal of Neurochirurgy. 2001;1: 3-16.

Crestani CC. Emotional stress and cardiovascular complications in animal models: A review of the influence of stress type. Front Physiol. 2016;7:251 doi: 10.3389/fphys.2016.00251.

Kellerová E. Variability and reactive changes of the peripheral blood flow, blood pressure and of the electrical behavior of the heart. Act. Nerv. Super. Rediviva. 2013; 55:113-124. ISSN 1337-933X

Mostofsky E, Maclure M, Sherwood JB, et al. Risk of acute myocardial infarction after the death of a significant person in one's life: the Determinants of Myocardial Infarction Onset Study. Circulation. 2012;125:491-496. doi: 10.1161/CIRCULATIONAHA.111.061770.

Nalivaiko E. Animal models of psychogenic cardiovascular disorders: what we can learn from them and what we cannot. Clin. Exp. Pharmacol. Physiol. 2011;38: 115-125.

Schwartz BG, French WJ, Mayeda GS, et al. Emotional stressors trigger cardiovascular events. Int. J. Clin. Pract. 2012;66:631-639. doi: 10.1111/j.1742-1241.2012.02920.x.

Struzkova K, Stourac P, Kanovsky J, et al. An unusual reason for severe bradycardia leading to cardiac arrest during general anaesthesia: a case repor. Biomed. Pap. Med. Fac. Univ. Palacky Olomouc Czech Repub. 2014;158:659-661. doi: 10.5507/bp.2013.005. Epub 2013 Mar 22.

Y-Hassan S, Feldt K, Stålberg M. A missed penalty kick triggered coronary death in the husband and broken heart syndrome in the wife. Am. J. Cardiol. 2015;116: 1639-1642. doi: 10.1016/j.amjcard.2015.08.033. Epub 2015 Sep 3.

Barbaryan A, Bailuc SL, Patel K, et al. An emotional stress as a trigger for reverse Takotsubo cardiomyopathy: a case report and literature review. Am. J. Case Rep. 2016;17:137-142. PMID: 26946334

Daiber A, Steven S, Weber A, et al. Targeting vascular (endothelial) dysfunction. Br. J. Pharmacol. 2016; doi: 10.1111/bph.13517.

Shliakhto E. V., Berkovich O. A., Beliaeva L. B. Modern concepts of endothelial dysfunction and methods of its correction in atherosclerosis. International neurological. Journal. 2002;3:9-13. (in Russian).

Esch T, Stefano GB, Fricchione GL, Benson H. Stress in cardiovascular diseases./ Med. Sci. Monit. 2002;8:A93-A101.

Sander M. Neural mechanisms in nitric-oxide-deficient hypertension. Curr. Opin. Nephrol. Hypertens. 1999;8:61-73.

Zicha J, Dobešová Z, Behuliak M, Pintérová M, Kuneš J, Vaněčková I. Nifedipine-sensitive blood pressure component in hypertensive models characterized by high activity of either sympathetic nervous system or renin-angiotensin system. Physiol. Res. 2014;63:13-26. PMID: 24397813

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, [4]:217-220. PMID: 27075385

Netliukh A. M. Dynamics of arginine levels in a hemorrhagic stroke due to ruptures of arterial aneurysms of the vessels of the brain. Lviv Medical Journal - Acta Medica Leopoliensia. 2013;2:4-7.

Zhao Y. Endothelial nitric oxide synthase-independent release of nitric oxide in the aorta of the spontaneously hypertensive rats. J. Pharmacol. Exp. Ther. 2012;344:15-22. doi: 10.1124/jpet.112.198721. Epub 2012 Sep 24.

Zhao X, Zhang LK, Zhang CY, et al. Regulatory effect of hydrogen sulfide on vascular collagen content in spontaneously hypertensive rats. Hypertens. Res. 2008;31:P. 1619-1630. DOI: 10.1291/hypres.31.1619

Drobna M, Misiak A, Holland T, et al. Captopril partially decreases the effect of H2S on rat blood pressure and inhibits H2S-induced nitric oxide release from S-nitrosoglutathione. Physiol Res. 2015;64:479-486. PMID: 25470515

Cacanyiova S., Berenyiova A., Kristek F. The Role of Hydrogen Sulphide in Blood Pressure Regulation. Physiol. Res. 2016;65[3]:273-289. PMID: 27775417

Wojtera M., Sikorska B., Sobow T., Liberski P.P. Microglial cells in neurodegenerative disorders. Folia Neuropathol. 2005;43:311–321.

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

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

Bucci M., Mirone V., Di Lorenzo A. et al. Hydrogen sulphide is involved in testosterone vascular effect. Eur. Urol. 2009;56:378–383. doi: 10.1016/j.eururo.2008.05.014. Epub 2008 May 22.

Kimura Y., Dargusch R., Schubert D., Kimura H. Hydrogen sulfide protects HT22 neuronal cells from oxidative stress. Antioxid. Redox. Signal. 2006;8:661–670. DOI: 10.1089/ars.2006.8.661

Bhatia Li L., Zhu Y.Z. et al. Hydrogen sulfide is a novel mediator of lipopolysaccharide-induced inflammation in the mouse. FASEB J. 2005;19:1196–1198.

Zhang H., Zhi L., Moore P.K., Bhatia M. Role of hydrogen sulfide in cecal ligation and puncture-induced sepsis in the mouse. Am. J. Physiol. Lung. Cell. Mol. Physiol. 2006;290:L1193–L1201. https://doi.org/10.1152/ajplung.00489.2005.

Song Y, Wang L. Hydrogen sulfide and acute lung injury.World Journal of Pharmacy and Pharmaceutical Sciences. 2016;5[12]:367-386. DOI: 10.20959/wjpps201612-7760.

Qi QY, Chen W, Li XL, Wang YW, Xie XH. H₂S protecting against lung injury following limb ischemia-reperfusion by alleviating inflammation and water transport abnormality in rats. Biomed. Environ. Sci. 2014;27[6]:410-418. doi: 10.3967/bes2014.070.

Ning J, Mo L, Zhao H, et al. Sodium Hydrosulphide alleviates remote lung injury following limb traumatic injury in rats. PLoS One. 2013;8[3] е59100.

Yang Lu, Lin J., Zhao Х. et al. Exogenous hydrogen sulfide restores cardiac function after trauma-hemorrhagic shock by inhibiting mitochondrial apoptosis. Int. J. Clin. Exp. Med. 2016; 9[3]:5563-5573. ISSN:1940-5901/IJCEM0019352

Payne JA, Reckelhoff JF, Khalil RA. Role of oxidative stress in age-related reduction of NO-cGMP-mediated vascular relaxation in SHR. Am. J. Physiol. Regul. Integr. Comp. Physiol. 2003;285:542-551.

Bernatova I. Endothelial dysfunction in experimental models of arterial hypertension: cause or consequence? Biomed. Res. Int. 2014; PubMed 598271.

Bachschmid MM, Schildknecht S, Matsui R, et al. Vascular aging: chronic oxidative stress and impairment of redox signaling-consequences for vascular homeostasis and disease. Ann. Med. 2013;45:17-36. doi: 10.3109/07853890.2011.645498. Epub 2012 Mar 1.

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.

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




DOI: https://doi.org/10.22141/2224-0586.3.90.2018.129480

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