Assessment of infusion therapy impact on the dynamics of endothelin-1 in patients with acute ischemic stroke
Keywords:stroke, solutions, endothelins, HES 130, HAES-LX-5 %, 0.9 % NaCl, mannitol
The impact of infusion solutions on endothelial damage correction in acute ischemic stroke (AIS) remains an insufficiently studied.
Purpose. To investigate the dynamics of endothelin-1 as one of the main markers of vasoconstriction and endothelial dysfunction (ED) with the use of 0.9 % NaCl, HES 130, HAES-LX-5 % and mannitol in patients with AIS.
Materials and methods. The study included 32 patients with AIS. As the investigated solutions were used: colloid hyperosmolar HAES-LX-5 % (Gecoton), colloid isoosmolar hydroxyethylstarch 6% 130/04 (HES 130), hyperosmolar mannitol 15 %, isoosmolar 0.9 % NaCl. The control group consisted of patients who received only 0.9 % NaCl, comparison group patients received 0.9% NaCl + HES 130 or 0.9 % NaCl + HAES-LX-5 %, or 0.9 % NaCl + mannitol. The level of endothelin-1 (EN-1) served as a vasoconstriction marker of ED at a fixed time (days 1, 4 and 7).
Results. Infusion therapy with only 0.9 % NaCl negatively affected the level of EN-1, since its level was 3.17 times increased on the 7th day of observation in comparison with the 4th day (P < 0.05). In the course of seven-day treatment with mannitol, a sharp increase in EN-1 serum level on average 3.73 and 3.48 times higher on day 7 (P < 0.05) compared to days 1 and 4, respectively, was observed. Infusion therapy with HES 130 and HAES-LX-5 % solutions produced a moderate depressing effect. So, the HAES-LX-5 % and HES 130 groups demonstrated a trend towards a decrease in ЕN-1 level (P > 0.05) at the end of observation in comparison with mannitol and 0.9 % NaCl groups, which showed a paradoxical increase in its level at the 7th day of infusion.
Conclusions. The dynamics of EN-1 level as the main vasoconstrictor marker of ED were negative in the group of patients with 0.9 % NaCl and mannitol: its level was 3.17 and 3.48 times increased in the 0.9 % NaCl and mannitol groups (P < 0,05), respectively, on day 7 compared to day 4 of observation. Intensive therapy with HAES-LX-5 % and HES 130 had a better depressing effect on an increase in EN-1 level than other solutions.
Appleton, J.P, Sprigg, N., Bath, P.M. (2016). Blood pressure management in acute stroke. Stroke Vasc Neurol, 1(2), 72–82. doi: 10.1136/svn-2016-000020.
Eskes, G. A., Lanctôt, K. L., Herrmann, N., Lindsay, P., Bayley, M., Bouvier, L., et al. (2015). Canadian Stroke Best Practice Recommendations: Mood, Cognition and Fatigue Following Stroke Practices Guidelines, update 2015. Int. J. Stroke, 10(7), 1130–40. doi: 10.1111/ijs.12557.
Sharma, R., Gowda, H., Chavan, S., Advani, J., Kelkar, D., Kumar, G. S., Bhattacharjee, M., et al. (2015). Proteomic Signature of Endothelial Dysfunction Identified in the Serum of Acute Ischemic Stroke Patients by the iTRAQ-Based LC-MS Approach. J. Proteome Res, 14(6), 2466–2479. doi: 10.1021/pr501324n.
Martí-Fàbregas, J., Delgado-Mederos, R., Crespo, J., Peña, E., Marín, R., Jiménez-Xarrié, E., et al. (2015). Circulating endothelial progenitor cells and the risk of vascular events after ischemic stroke. PLoS One, 10(4), e0124895. doi: 10.1371/journal.pone.0124895.
Katerhenchuk, I. P. (2015). Klinichna otsinka, diahnostychne ta prohnostychne znachennia rezultativ laboratornykh doslidzhen. Chastyna 1: Kardiolohiia [Clinical evaluation, diagnostic and prognostic value of the results of laboratory research. Part 1: Cardiology]. Poltava: Medknyha. [in Ukrainian].
Domashenko, M. A., Orlov, S. V., Kostyreva, M. V., Tanashyan, М. M., lonova, V. G., & Suslina, Z. A. (2007). Sostoyanie funkcii e'ndoteliya pri ishemicheskikh narusheniyakh mozgovogo krovoobrascheniya [The endothelial functional status in patients with ischemic cerebrovascular disorders]. Nevrologicheskij zhurnal, 12(6), 10–14. [in Russian].
Ryabchenko, А. Yu., Dolgov, A. М., Denisov, Е. N., & Gumanova, N. G. (2014). Rol' oksida azota i e'ndotelina-1 v razvitii ishemicheskikh narushenij mozgovogo krovoobrascheniya [Role of nitric oxide and endothelin-1 in the development of ischemic disorders of cerebral circulation]. Nevrologicheskij vestnik. Zhurnal im. V.M. Behtereva, 46(1), 34–37. [in Russian].
Peng, Q., Huang, Y., Sun, W., & Xing, H. (2014). Associations among cerebral microbleeds, cerebral large-artery diseases and endothelial function. Chin. Med. J. (Engl). 127(18), 3204–3208.
Gumanova, N.G., Teplova, N.V., Ryabchenko, A.U., & Denisov, E.N. (2015). Serum nitrate and nitrite levels in patients with hypertension and ischemic stroke depend on diet: a multicenter study. Clin. Biochem, 48(1–2), 29–32. doi: 10.1016/j.clinbiochem.2014.10.010.
Shin, H. K., Oka, F., Kim, J. H., Atochin, D., Huang, P. L., & Ayata, C. (2014). Endothelial dysfunction abrogates the efficacy of normobaric hyperoxia in stroke. J. Neurosci, 34(46), 15200–15207. doi: 10.1523/JNEUROSCI.1110-14.2014.
García-Pastor, A., Díaz-Otero, F., Funes-Molina, C., Benito-Conde, B., Grandes-Velasco, S., Sobrino-García, P., et al. (2015). Tissue plasminogen activator for acute ischemic stroke: calculation of dose based on estimated patient weight can increase the risk of cerebral bleeding. J. Thromb. Thrombolysis, 40(3), 347–52. doi: 10.1007/s11239-015-1232-4.
Brodoehl, S., Günther, A., Witte, O. W., & Klingner, C. M. (2015). How to manage thrombolysis interruptions in acute stroke? Clin. Neuropharmacol, 38(3), 85–88. doi: 10.1097/WNF.0000000000000081.
Tsivgoulis, G., Sharma, V. K., Mikulik, R., Krogias, C., Haršány, M., Bavarsad Shahripour, R., et al. (2014). Intravenous thrombolysis for acute ischemic stroke occurring duriццng hospitalization for transient ischemic attack. Int. J. Stroke, 9(4), 413–418. doi: 10.1111/ijs.12125.
Oddo, M., Poole, D., Helbok, R., Meyfroidt, G., Stocchetti, N., Bouzat, P., et al. (2018). Fluid therapy in neurointensive care patients: ESICM consensus and clinical practice recommendations. Intensive Care Med, 44(4), 449–463. doi: 10.1007/s00134-018-5086-z.
Kurovska, V. O. (2012). Patohenetychni kryterii dyferentsiatsii roli NO-zalezhnykh mekhanizmiv v ishemichnykh i reperfuziinykh poshkodzhenniakh holovnoho mozku (Avtoref. dis…kand. med. nauk). [Pathogenetic Criteria for Differentiation of NO-Fallow Mechanisms in the Inhumous and Reperfusion Poses of the Brain] (Extended abstract of candidate’s thesis). Chernivtsi. [in Ukrainian].
Semenenko, A. I. (2013). Dynamika aktyvnosti neiron-spetsyfichnoi enolazy ta vmistu bilka S 100 u krovi schuriv za umov hostroho porushennia mozkovoho krovoobihu ta kursovoho vvedennia 0,9% rozchynu NaCl [The dynamics of neuron specific enolase activity and protein S 100 level in rat's blood under of acute disorder of the cerebral circulation and course intravenous injection of 0,9% solution NaCl]. Farmakolohiia ta likarska toksykolohiia, 6(36), 9–13. [in Ukrainian].
Semenenko, A. I. (2016). Aktyvnist neiron-spetsyfichnoi enolazy u patsientiv z hostrym ishemichnym insultom na foni korektsii infuziinymy rozchynamy [Act ivity of neuron-specific enolase in patient s with ac ute ischemic stroke on the background of correction of infusion solut ions]. Bil, znebolennia i intensyvna terapiia, 4(77), 52–58. [in Ukrainian]. doi: https://doi.org/10.25284/2519-2078.4(77).2016.94295.
How to Cite
LicenseAuthors 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)