Dexmedetomidine Increases the Latency of Thermal Antinociception in Rats

Tsutsui, Yukako; Sunada, Katsuhisa

doi:10.2344/anpr-65-01-08

Cited by 3 publications

(2 citation statements)

References 18 publications

(6 reference statements)

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“…In order to measure the local anesthetic effect, the thermal nociceptive block assessment protocol reported by Tsutsui et al 10 was implemented. First, a rat was placed in a wire net container, which was placed on a heated glass base.…”

Section: Methodsmentioning

confidence: 99%

“…The subject sample size was calculated using G*Power software version 3.1.9.2 (E. Erdfelder, Psychologicsches Institute der Universitat Dusseldorf, Germany) with an α error probability of .05, a power of 0.8, and an effect size based on a mean difference in paw withdrawal latency of 3.0 seconds (SD 3.0 seconds) for each group. The estimate of the difference in paw withdrawal latency used for this analysis was obtained from a previous study by Tsutsui et al 10 Based on these parameters, the power analysis demonstrated that 44 rats in total or 11 rats per group were required for this study.…”

Section: Methodsmentioning

confidence: 99%

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

Tsutsui

Sunada

2020

Anesthesia Progress

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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.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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

Tsutsui

Sunada

2020

Anesthesia Progress

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Anesthesia and analgesia in laboratory rodents

Jirkof

Lofgren²

2023

Anesthesia and Analgesia in Laboratory Animals

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Photogenetics Inhibits the Activity of Glutamate Neurons Projected from the Motor Cortex to the Ventroposterolateral Nucleus of the Thalamus to Alleviates Central Post-Stroke Pain in Rats

Deng,

Gu,

2024

Preprint

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The "central sensitization" and "central imbalance" theories suggest that central post-stroke pain (CPSP) is the result of neuronal overactivity and an imbalance between excitatory and inhibitory functions of the nervous system caused by damage to the sensory system. The ventral posterior lateral nucleus of the thalamus (VPL) and the primary motor cortex (M1) are key brain regions for nociceptive message transmission. However, the effects of inhibiting M1-VPL glutamatergic projections in CPSP remain unclear. his study investigates the efficacy of photogenetic inhibition of M1-VPL glutamatergic neuron excitability in a rat model of CPSP. CPSP rats underwent M1 injection with rAAV encoding an inhibitory photosensitive protein, followed by implantation of an optical fiber sleeve above the VPL and subsequent 10 W, 20 Hz, 5 ms yellow laser (589 nm) irradiation. The irradiation scheme was to start from the 3rd day after the CPSP mode, light for 2 min, turn off for 3 min, and repeat 6 times a day for 12 consecutive days. We observed that the mechanical and thermal pain thresholds were increased in CPSP rats, and the expressions of M1 pain-related factors c-Fos, vesicular glutamate transporter protein 2 (VGLUT2), and N-methyl-D-aspartate receptor subtype 2B (NR2B) were down-regulated. These findings indicate that photogenetic inhibition of M1-VPL glutamatergic projection can relieve pathologic pain in CPSP rats.

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Dexmedetomidine Increases the Latency of Thermal Antinociception in Rats

Cited by 3 publications

References 18 publications

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

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

Anesthesia and analgesia in laboratory rodents

Photogenetics Inhibits the Activity of Glutamate Neurons Projected from the Motor Cortex to the Ventroposterolateral Nucleus of the Thalamus to Alleviates Central Post-Stroke Pain in Rats

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