Dexmedetomidine (DEX) is a sedative and analgesic agent that acts via the alpha-2 adrenoreceptor and is associated with reduced anesthetic requirements, as well as attenuated blood pressure and heart rate in response to stressful events. A previous study reported that cat gingival blood flow was controlled via sympathetic alpha-adrenergic fibers involved in vasoconstriction. In the present study, experiment 1 focused on the relationship between the effects of DEX on alpha adrenoreceptors and vasoconstriction in the tissues of the oral cavity and compared the palatal mucosal blood flow (PMBF) in rabbits between general anesthesia with sevoflurane and sedation with DEX. We found that the PMBF was decreased by DEX presumably because of the vasoconstriction of oral mucosal vessels following alpha-2 adrenoreceptor stimulation by DEX. To assess if this vasoconstriction would allow decreased use of locally administered epinephrine during DEX infusion, experiment 2 in the present study monitored the serum lidocaine concentration in rabbits to compare the absorption of lidocaine without epinephrine during general anesthesia with sevoflurane and sedation with DEX. The depression of PMBF by DEX did not affect the absorption of lidocaine. We hypothesize that this is because lidocaine dilates the blood vessels, counteracting the effects of DEX. In conclusion, despite decreased palatal blood flow with DEX infusion, local anesthetics with vasoconstrictors should be used in implant and oral surgery even with administered DEX.
Preparation for experiment 1. General anesthesia in both groups was induced and maintained with sevoflurane in oxygen for a tracheotomy and placement of femoral artery and vein catheters. Then, a laser Doppler flowmeter probe (ALF21RTM; Advance, Tokyo, Japan) was fixed onto the palatal mucosal surface using a piece of sponge to monitor the palatal mucosal blood flow (PMBF) continuously. After the preparation (tracheotomy and placement of catheters), at least 5 minutes elapsed until the cardiovascular parameters had stabilized when control (time 0) measurements were made.
Time course of experiment 1. Mean arterial pressure (MAP), heart rate (HR), central venous pressure (CVP), end-tidal CO2 (ETCO2), and palatal mucosal blood flow (PMBF) were measured in both groups at 12, 17, 22, 27, 32, and 42 minutes after administration of 0.2 mg/kg midazolam, 0.05 mg/kg butorphanol, and 2 mg/kg rocuronium (time 0). The SMB group was maintained with sevoflurane in oxygen. The DMB group was maintained with dexmedetomidine. SMB indicates sevoflurane, midazolam, and butorphanol; DMB, dexmedetomidine, midazolam, and butorphanol.
Preparation for experiment 2. General anesthesia in both groups was induced and maintained with sevoflurane in oxygen for a tracheotomy. A 3-Fr catheter was then inserted via the femoral artery with the tip placed in the thoracic aorta to take blood samples.
Time course of the investigation in experiment 2. Experiment 2 followed the same anesthetic protocol as experiment 1, except that in both the SMB and DMB groups, 0.5 mL of 2% lidocaine without adrenaline was injected submucosally into both the right and left palatal mucosa (total 20 mg) at 12 minutes after administration of 0.2 mg/kg midazolam, 0.05 mg/kg butorphanol, and 2 mg/kg rocuronium (time 0). Three milliliters of blood samples were then taken at 17, 22, 27, 32, and 42 minutes. SMB indicates sevoflurane, midazolam, and butorphanol; DMB, dexmedetomidine, midazolam, and butorphanol.
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