In vitro vasoactive effects of dexmedetomidine on isolated human umbilical arteries

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dc.contributor.authorArun, O.
dc.contributor.authorTaylan, S. B.
dc.contributor.authorDuman, I
dc.contributor.authorOc, B.
dc.contributor.authorYilmaz, S. A.
dc.contributor.authorTekin, A.
dc.contributor.authorCelik, C.
dc.date.accessioned2024-02-23T14:37:59Z
dc.date.available2024-02-23T14:37:59Z
dc.date.issued2019
dc.departmentNEÜen_US
dc.description.abstractOBJECTIVE: We aimed to investigate the vasoactive effects of dexmedetomidine on isolated human umbilical arteries and possible mechanisms involved. METHODS: Human umbilical artery strips were suspended in Krebs-Henseleit solution and dose-response curves were obtained for cumulative dexmedetomidine before and after incubation with different agents; propranolol, atropine, yohimbine, prazosin, indomethacin, verapamil. Effects of calcium on cumulative dexmedetomidine-induced contractions were also studied. RESULTS: Cumulative dexmedetomidine resulted in dose dependent contraction responses. Incubation with propranolol (Emax: 93.3 +/- 3.26 %), atropine (Emax: 92.0 +/- 6.54 %), or indomethacin (Emax: 94.25 +/- 2.62 %), did not attenuate dexmedetomidine-elicited contractions (p > 0.05). There were significant decreases in the contraction responses of cumulative dexmedetomidine with yohimbine (Emax: 12.1 +/- 11.9 %), prazosin (Emax: 28.8 +/- 4.6 %) and verapamil (Emax: 11.2 +/- 13.6 %) (p < 0.05). In Ca+2 free medium contraction responses to cumulative dexmedetomidine was insignificant (Emax: 5.20 +/- 3.42 %). Addition of cumulative calcium to the Ca+2 free medium resulted in concentration dependent increase in contractions (Emax: 64.83 +/- 37.7 %) (p < 0.05). CONCLUSION: Dexmedetomidine induces vasoconstriction in endothelial-free umbilical arteries via both, alpha(1)- and alpha(2)-adrenergic receptors and also extracellular Ca+2 concentrations play a major role. beta-adrenergic receptors, muscarinic cholinergic receptors, and inhibition of cyclooxygenase enzyme are not involved in this vasoconstriction (Fig. 3, Ref. 36). Text in PDF www.elis.sk.en_US
dc.identifier.doi10.4149/BLL_2019_006
dc.identifier.endpage45en_US
dc.identifier.issn0006-9248
dc.identifier.issn1336-0345
dc.identifier.issue1en_US
dc.identifier.pmid30685991en_US
dc.identifier.scopus2-s2.0-85060648204en_US
dc.identifier.scopusqualityQ3en_US
dc.identifier.startpage40en_US
dc.identifier.urihttps://doi.org/10.4149/BLL_2019_006
dc.identifier.urihttps://hdl.handle.net/20.500.12452/16320
dc.identifier.volume120en_US
dc.identifier.wosWOS:000457596700007en_US
dc.identifier.wosqualityQ3en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherComenius Univen_US
dc.relation.ispartofBratislava Medical Journal-Bratislavske Lekarske Listyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectAlpha Adrenergic Receptorsen_US
dc.subjectDexmedetomidineen_US
dc.subjectIn Vitroen_US
dc.subjectUmbilical Corden_US
dc.subjectVascular Smooth Muscleen_US
dc.titleIn vitro vasoactive effects of dexmedetomidine on isolated human umbilical arteriesen_US
dc.typeArticleen_US

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