Adding Dexmedetomidine to Articaine Increases the Latency of Thermal Antinociception in Rats

Abstract

<jats:p>Articaine is a low-toxicity local anesthetic that is widely used in dentistry. Typically, epinephrine is added to prolong the duration of articaine local anesthesia; however, epinephrine exhibits adverse effects. Low-dose dexmedetomidine (DEX), an α2-adrenoreceptor agonist, reportedly prolongs local anesthesia without notable adverse cardiovascular effects. The purpose of this study was to assess whether a combination of low-dose DEX and articaine would provide a low-toxicity local anesthetic option for dental procedures without adverse cardiovascular effects. Thus, this study investigated whether DEX could prolong the local anesthetic effect of articaine using a rat model of pain. Adult male Wistar rats (N = 44; 11 per group) received a 50-μL subcutaneous injection into the plantar surface of the hind paws; injections were composed of either normal saline, 4% articaine (2 mg articaine), combined 5 μg/kg DEX and 4% articaine (1.25 μg DEX + 2 mg articaine), or combined epinephrine (1:100,000) and 4% articaine (0.9 μg epinephrine + 2 mg articaine). Subsequent acute pain perception was determined by paw withdrawal movement in response to infrared radiant heat stimulation of the plantar region. Paw withdrawal latency was tested at 5-minute intervals. Paw withdrawal latency values at 35 and 40 minutes were 3.83 ± 1.76 and 3.29 ± 1.43 seconds for articaine alone, 7.89 ± 2.72 and 7.25 ± 3.37 seconds for DEX and articaine, and 8.95 ± 2.28 and 8.17 ± 3.01 seconds for epinephrine and articaine. DEX prolonged the paw withdrawal latency of articaine for up to 35 minutes (p = .015) but not 40 minutes after injection (p = .052) when compared to articaine alone. The combination of DEX and articaine can provide effective local anesthesia for up to 35 minutes after injection.</jats:p>

Inhibitory Actions of Clinical Analgesics, Analgesic Adjuvants, and Plant-Derived Analgesics on Nerve Action Potential Conduction

“…This is possibly due to the inhibition produced by the agonists of excitatory transmission mediated by glutamate in spinal superficial dorsal horn neurons [247]. Administration of α 2 adrenoceptor agonists and local anesthetics for the purpose of spinal anesthesia prolongs peripheral nerve conduction block in animals [248][249][250][251] and humans ( [252][253][254][255][256][257][258][259]; refer to review [260]). This is possibly due to a local vessel contraction produced by the agonists, leading to decreased removal of the anesthetics from the subarachnoid space [261,262].…”