• Reg Anesth Pain Med · Mar 2014

    Locally Injected Dexmedetomidine Induces Vasoconstriction via Peripheral α-2A Adrenoceptor Subtype in Guinea Pigs.

    • Akiko Yabuki, Hitoshi Higuchi, Tatsushi Yoshitomi, Yumiko Tomoyasu, Minako Ishii-Maruhama, Shigeru Maeda, and Takuya Miyawaki.
    • From the *Department of Dental Anesthesiology and Special Care Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences; †Department of Dental Anesthesiology, Okayama University Hospital; and ‡Dental Clinic, Okayama Kyoritsu General Hospital, Okayama, Japan.
    • Reg Anesth Pain Med. 2014 Mar 1;39(2):133-6.

    Background And ObjectivesRecent research shows that locally injected dexmedetomidine enhances the local anesthetic potency of lidocaine via the α-2A adrenoceptor subtype in guinea pigs. However, little is known about the effect of locally injected dexmedetomidine on the peripheral vascular response. This study aimed to evaluate the effect of locally injected dexmedetomidine on the peripheral vascular response, measuring skin blood flow in the injected area in guinea pigs.MethodsDexmedetomidine was intracutaneously injected at a volume of 0.1 mL into the backs of guinea pigs, and further injected combined with yohimbine, a selective antagonist of α-2 adrenoceptors, or prazosin, a selective antagonist of α-1 adrenoceptors and an antagonist of both α-2B and α-2C adrenoceptor subtypes. Skin blood flow was measured until 60 minutes after injection using a laser-Doppler flowmeter. Furthermore, systemic arterial blood pressure and pulse of the guinea pigs were monitored via a catheter inserted into the carotid artery throughout every experiment.ResultsDexmedetomidine at a concentration of 1 μM significantly decreased the skin blood flow in a dose-dependent manner with no changes in the mean blood pressure and pulse. Yohimbine completely antagonized the effect of dexmedetomidine, but prazosin did not.ConclusionsThe results reveal that locally injected dexmedetomidine at a concentration of 1 μM induced peripheral vasoconstriction without a systemic cardiovascular response via the peripheral α-2A adrenoceptor subtype.

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