• J. Cardiothorac. Vasc. Anesth. · Oct 2007

    Dexmedetomidine produces dual alpha2-adrenergic agonist and alpha1-adrenergic antagonist actions on human isolated internal mammary artery.

    • Oguzhan Yildiz, Hasan B Ulusoy, Melik Seyrek, Husamettin Gul, and Vedat Yildirim.
    • Department of Pharmacology, Gulhane School of Medicine, Ankara, Turkey. oyildiz@gata.edu.tr
    • J. Cardiothorac. Vasc. Anesth. 2007 Oct 1; 21 (5): 696-700.

    ObjectiveTo investigate the direct effects of dexmedetomidine (DEX) on isolated human internal mammary artery (IMA).DesignIn vitro experimental study.SettingCardiovascular Pharmacology Laboratory, Department of Pharmacology, Gulhane School of Medicine, Ankara, Turkey.ParticipantsIMA segments were obtained from 18 patients undergoing coronary artery bypass surgery.InterventionsThe response in IMA was recorded isometrically by a force displacement transducer in isolated organ baths. DEX-induced contractions were tested in the presence of the alpha2-adrenoceptor antagonist yohimbine (10(-7) mol/L) and the alpha1-adrenoceptor antagonist prazosin (10(-8) M). The effect of DEX (10(-7), 10(-6), and 10(-5) mol/L) on phenylephrine (10(-9)-3 x 10(-4) mol/L)-induced contactions was also tested.Measurement And Main ResultsDEX (10(-9) mol/L-3 x 10(-5) mol/L) caused contraction in IMA segments. The contraction at lower concentrations of DEX (10(-9) mol/L-3 x 10(-7) mol/L) was attenuated by yohimbine (10(-7) mol/L), whereas prazosin (10(-8) mol/L) attenuated the contractions at higher concentrations of DEX (10(-6) mol/L-3 x 10(-5) mol/L). Incubation of IMA segments with high concentrations of DEX (10(-6) mol/L and 10(-5) mol/L) caused an inhibition of phenylephrine (10(-9) mol/L-3 x 10(-4) mol/L)-induced contraction.ConclusionThese data suggest that DEX causes contraction by activating alpha2-adrenoceptors at lower concentrations, but it may also activate alpha1-adrenoceptors at higher concentrations in IMA. The action of DEX on phenylephrine-induced contraction may be related to an alpha1-adrenoceptor antagonistic effect produced via partial alpha1-adrenoceptor agonistic action.

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