PT  - JOURNAL ARTICLE
AU  - Akiko Yabuki
AU  - Hitoshi Higuchi
AU  - Tatsushi Yoshitomi
AU  - Yumiko Tomoyasu
AU  - Minako Ishii-Maruhama
AU  - Shigeru Maeda
AU  - Takuya Miyawaki
TI  - Locally Injected Dexmedetomidine Induces Vasoconstriction via Peripheral α-2A Adrenoceptor Subtype in Guinea Pigs
AID  - 10.1097/AAP.0000000000000048
DP  - 2014 Mar 01
TA  - Regional Anesthesia & Pain Medicine
PG  - 133--136
VI  - 39
IP  - 2
4099  - http://rapm.bmj.com/content/39/2/133.short
4100  - http://rapm.bmj.com/content/39/2/133.full
SO  - Reg Anesth Pain Med2014 Mar 01; 39
AB  - Background and Objectives Recent 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.Methods Dexmedetomidine 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.Results Dexmedetomidine 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.Conclusions The 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.