The contribution of red blood cell microrheological characteristics to impaired blood fluidity in peripheral arterial occlusive disease (PAOD) and their correction with gasotransmitters
E. Volkova, A. Zamyshlyaev
, A. I. Tikhomirova
, A. Kolobanov, V. Gerasenkov, A. Muravyov
, N. Antonova
, I. Velcheva
Резюме: Objective: Peripheral arterial occlusive disease (POAD) is a pathology in which the artery dilatation reserve is reduced. Therefore, the rheological properties of the blood can either compensate for or worsen this vascular problem. The purpose of this study was to investigate the possibility of restoring normal microrheological values of red blood cells (RBCs) in patients with PAOD using gasotransmitter (GT) donors and substrates for their synthesis. Materials and methods: In healthy individuals (group 1, men, n=24) and patients with POAD (group 2, men, n=20), the characteristics of hemorheological profiles were recorded. Deformability of RBC (RBCD) and aggregation (RBCA) after cell incubation with GT donors: H2S (NaHS), NO (SNP) or substrates for their synthesis (L-arginine and L-cysteine) were measured. Results: In patients with POAD, a decrease in blood fluidity was observed due to an increase in plasma viscosity, RBCA and a decrease in RBCD. It was found that RBCD makes a greater contribution to the change in blood fluidity. GT donors and their synthesis substrates moderately increased RBCD (p<0.01) and significantly decreased RBCA (p<0.01) in both groups.
Discussion: It has been shown that deteriorated RBCD and high RBCA can be restored to normal values with the help of gasotransmitters. Moreover, a greater positive microrheological effect was observed when two gasotransmitters were used together.
Series on Biomechanics, Vol.38, No.2 (2024), 3-10
DOI: 10.7546/SB.01.02.2024
Ключови думи: blood fluidity; gasotransmitters; microrheology; Peripheral arterial occlusive disease; red blood cells
Литература: (click to open/close) | [1] Schumann, R., Rieger, J., Ludwig, M., 2007. Akute periphere arterielle Verschlusskrankheit [Acute peripheral arterial occlusive disease]. Med Klin (Munich) 102,6, 457-71; quiz 472-3. doi: 10.1007/s00063-007-1059-7. [2] Kiesewetter, H., Jung, F., Blume, J., Spitzer, S., Birk, A., 1991. Hyper- oder isovolämische Hämodilution bei Patienten mit peripherer arterieller Verschlusskrankheit im Stadium II [Hyper- or isovolemic hemodilution in patients with stage II peripheral arterial occlusive disease]. Acta Med Austriaca 18 Suppl 1, 23-7. [3] Kiesewetter, H., Jung, F., 1984. Hämorheologische Therapie bei peripherer arterieller Verschlusskrankheit [Hemorheologic therapy in peripheral arterial occlusive disease]. Fortschr Med 102, 37, 921-4. [4] Angelkort, B., 1986. Blutrheologie bei peripherer Verschlusskrankheit. Effekte von Hämodilution und Pentoxifyllin [Blood rheology in peripheral occlusive disease. Effects of hemodilution and pentoxifylline]. Wien Med Wochenschr 136 Spec No, 29-35. [5] Schütz, R.M., 1992. Aktuelle Therapie bei peripheren arteriellen Durchblutungsstörungen im Alter [Current therapy of peripheral arterial occlusive diseases in the aged]. Z Gerontol 25, 2, 101-4. [6] Sternitzky, R., Seige, K., 1983. Hämorheologische Veränderungen und ihre klinische Bedeutung bei chronisch-arterieller Verschlusskrankheit [Blood rheological changes and their clinical significance in chronic arterial obstructive disease]. Z Gesamte Inn Med 38, 1,1-7. [7] Pinho, D., Carvalho, V., Gonçalves, I.M., Teixeira, S., Lima, R., 2020. Visualization and Measurements of Blood Cells Flowing in Microfluidic Systems and Blood Rheology: A Personalized Medicine Perspective. J Pers Med 10, 4, 249. doi: 10.3390/jpm10040249. [8] Muravyov, A.V., Tikhomirova I.A., 2013. Role molecular signalling pathways in changes of red blood cell deformability. Clin Hemorheol Microcirc 53, 1-2, 45-59. doi: 10.3233/CH-2012-1575. [9] Ugurel, E., Goksel, E., Cilek, N., Kaga, E., Yalcin, O., 2022. Proteomic Analysis of the Role of the Adenylyl Cyclase-cAMP Pathway in Red Blood Cell Mechanical Responses. Cells 11, 7, 1250. doi: 10.3390/cells11071250. [10] Cilek, N., Ugurel, E., Goksel, E., Yalcin, O., 2024. Signaling mechanisms in red blood cells: A view through the protein phosphorylation and deformability. J Cell Physiol 239, 3, e30958. doi: 10.1002/jcp.30958. [11] Grau, M., Pauly,S., Ali, J., Walpurgis, K., Thevis, M., Bloch, W., Suhr F., 2013. RBC-NOS-dependent S-nitrosylation of cytoskeletal proteins improves RBC deformability. PLoS One 8(2), e56759. doi: 10.1371/journal.pone.0056759. [12] Mozar, A., Connes, P., Collins, B., Hardy-Dessources, M.D., Romana, M., Lemonne, N., Bloch, W., Grau, M., 2016. Red blood cell nitric oxide synthase modulates red blood cell deformability in sickle cell anemia. Clin. Hemorheol. Microcirc 64, 47-53. doi: 10.3233/CH-162042. [13] Muravyov, A.V., Tikhomirova, I.A., Avdonin, P.V., Bulaeva, S.V., Malysheva, Yu.V., Kislov, N.V., 2019. Cellular models of erythrocytes for studying the effect of gasotransmitters on their microrheology. Journal of Cellular Biotechnology 5, 1, 3-10. doi: 10.3233/JCB-189009. 1. [14] Dintenfass, L., 1981. Clinical applications of heamorheology. The Rheology of blood, blood vessels and associated tissues New York, Oxford Press, 22–50. [15] Stoltz, J.F., Donner, M., Muller, S., Larcan, A., 1991. Hemorheology in clinical practice. Introduction to the notion of hemorheologic profile J. Mal. Vasc. 6, 261-270. [16] Muravyov, A.V., Antonova, N., Tikhomirova, I.A., 2019. Red blood cell micromechanical responses to hydrogen sulfide and nitric oxide donors: Analysis of crosstalk of two gasotransmitters (H2S and NO). Series on Biomechanics 33, 2, 34-40. [17] Angelkort B., Boateng K., Maurin N., 1980. Blood fluidity and coagulation phenomena in chronic arterial occlusive disease. J Int Med Res 8, 3, 242-6. doi: 10.1177/030006058000800310 [18] Forconi, S., Guerrini M., 1996. Do hemorheological laboratory assays have any clinical relevance? Clin. Hemorheol 16, 1, 17–21. [19] Ugurel, E., Kisakurek, Z.B., Aksu, Y., Goksel, E., Cilek, N., Yalcin, O., 2021. Calcium/protein kinase C signaling mechanisms in shear-induced mechanical responses of red blood cells. Microvasc Res 135, 104124. doi: 10.1016/j.mvr.2020.104124. [20] DiCarlo, A.L., Holdsworth, D.W., Poepping, T.L., 2019. Study of the effect of stenosis severity and non-Newtonian viscosity on multidirectional wall shear stress and flow disturbances in the carotid artery using particle image velocimetry. Med Eng Phys 65, 8-23. doi: 10.1016/j.medengphy.2018.12.023. [21] Wilkinson, W.L., 1964 Wilkinson Non-Newtonian fluids. New York–london: Pergamon Press. [22] Schäbitz J., 1982. Zur Bedeutung der Hämorheologie in der Inneren Medizin [The importance of hemorheology in internal medicine]. Z Gesamte Inn Med 37, 12, 372-8. [23] Pries, A.R., Secomb T.W., 1997. Resistance to blood flow in vivo: from Poiseuille to the «in vivo viscosity law». Biorheology 34(4-5), 369–373. doi.org/10.1016/S0006-355X (98)00011-0. [24] Hamlin, S.K., Benedik, P.S., 2014. Basic concepts of hemorheology in microvascular hemodynamics. Crit Care Nurs Clin North Am 26, 3, 337-44. doi: 10.1016/j.ccell.2014.04.005. [25] Minetti, G., Ciana A., Balduini C., 2004. Differential sorting of tyrosine kinases and phosphotyrosine phosphatases acting on band 3 during vesiculation of human erythrocytes. Biochem J 377, 489-497. doi: 10.1042/BJ20031401. [26] Saldanha, C., Silva, A.S., Gonçalves, S., Martins-Silva, J., 2007. Modulation of erythrocyte hemorheological properties by band 3 phosphorylation and dephosphorylation. Clin. Hemorheol. and Microcirc 36, 183-194. [27] Uyuklu, M., Meiselman, H.J., Baskurt, O.K., 2009. Role of hemoglobin oxygenation in the modulation of red blood cell mechanical properties by nitric oxide. Nitric Oxide 21, 1, 20-26. doi: 10.1016/j.niox.2009.03.004. [28] Petrov, V., Lijnen P., 1996. Regulation of human erythrocyte Na+/H+ exchange by soluble and particulate guanylate cyclase. Am J Physiol 271, 1556-1564. doi: 10.1152/ajpcell.1996.271.5.C1556. [29] Coletta, C., Papapetropoulos, A., Erdelyi, K., Olah, G., Módis, K., Panopoulos, P., Asimakopoulou, A., Gerö, D., Sharina, I., Martin, E., Szabo., C., 2012. Hydrogen sulfide and nitric oxide are mutually dependent in the regulation of angiogenesis and endothelium-dependent vasorelaxation. Proc Natl Acad Sci U S A 5;109, 23, 9161-6. doi: 10.1073/pnas.1202916109. [30] Wu, D., Hu, Q., Zhu, D., 2018. An Update on Hydrogen Sulfide and Nitric Oxide Interactions in the Cardiovascular System. Oxid Med Cell Longev 4579140. doi: 10.1155/2018/4579140. [31] Marini, E., Rolando, B., Sodano, F., Blua, F., Concina, G., Guglielmo., S, Lazzarato, L., Chegaev, K., 2023. Comparative Study of Different H2S Donors as Vasodilators and Attenuators of Superoxide-Induced Endothelial Damage. Antioxidants (Basel). 2023;12, 2, 344. doi: 10.3390/antiox12020344. [32] Bucci, M., Papapetropoulos, A., Vellecco, V., Zhou, Z., Pyriochou, A., Roussos, C., Roviezzo, F., Brancaleone, V., Cirino, G., 2010. Hydrogen sulfide is an endogenous inhibitor of phosphodiesterase activity. Arterioscler Thromb Vasc Biol 30, 10, 1998-2004. doi: 10.1161/ATVBAHA.110.209783. [33] Searcy, D.G., Lee, S.H., 1998. Sulfur reduction by human erythrocytes. J Exp Zool 282, 3, 310-22. doi: 10.1002/(sici)1097-010x (19981015)282:3< 310: aid-jez4>3.0.co;2-p. [34] Andrés, CMC., Pérez de la Lastra, J.M., Andrés Juan C., Plou F.J., Pérez-Lebeña E., 2023. Chemistry of Hydrogen Sulfide-Pathological and Physiological Functions in Mammalian Cells. Cells 12, 23, 2684. doi: 10.3390/cells12232684. [35] Kimura, H., 2011. Hydrogen sulfide: Its production, release and functions. Amino Acids 41, 113–121. doi: 10.1007/s00726-010-0510-x.
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| Дата на публикуване: 2024-08-01
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