Antinociceptive Effects of Phenobarbital in ???Tail-Flick??? Test and Deafferentation Pain

Jm, González-Darder; Ortega-Álvaro, A.; Ruz-Franzi, I; Segura-Pastor, Dolores

doi:10.1213/00000539-199207000-00015

Cited by 9 publications

(7 citation statements)

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“…We have previously shown that various anxiolytic drugs interfering with the GABA-A receptor, including barbiturates, could induce a state of hyperalgesia (7), although the literature about this subject may be considered controversial (8,9). Extending data from previous work (7), in the present study we showed that acute phenobarbital administration induced a dose-dependent hyperalgesia.…”

Section: Discussionsupporting

confidence: 75%

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Acute phenobarbital administration induces hyperalgesia: pharmacological evidence for the involvement of supraspinal GABA-A receptors

Yokoro

Pesquero

Turchetti-Maia

et al. 2001

Braz J Med Biol Res

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The aim of the present study was to determine if phenobarbital affects the nociception threshold. Systemic (1-20 mg/kg) phenobarbital administration dose dependently induced hyperalgesia in the tail-flick, hot-plate and formalin tests in rats and in the abdominal constriction test in mice. Formalin and abdominal constriction tests were the most sensitive procedures for the detection of hyperalgesia in response to phenobarbital compared with the tail-flick and hot-plate tests. The hyperalgesia induced by systemic phenobarbital was blocked by previous administration of 1 mg/kg ip picrotoxin or either 1-2 mg/kg sc or 10 ng icv bicuculline. Intracerebroventricular phenobarbital administration (5 µg) induced hyperalgesia in the tail-flick test. In contrast, intrathecal phenobarbital administration (5 µg) induced antinociception and blocked systemic-induced hyperalgesia in this test. We suggest that phenobarbital may mediate hyperalgesia through GABA-A receptors at supraspinal levels and antinociception through the same kind of receptors at spinal levels.

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Section: Discussionsupporting

confidence: 75%

“…In addition, activation of the GABA-A receptor has been associated with pain modulation in the central nervous system (CNS), essentially through the descending inhibitory system (5). However, it is still a matter of discussion in the literature whether barbiturates increase (6,7) or decrease (8,9) the pain threshold.…”

Section: Introductionmentioning

confidence: 99%

Acute phenobarbital administration induces hyperalgesia: pharmacological evidence for the involvement of supraspinal GABA-A receptors

Yokoro

Pesquero

Turchetti-Maia

et al. 2001

Braz J Med Biol Res

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“…Analgesia, hyperalgesia or no effect has been attributed to these drugs (13)(14)(15)(16)(17)(18)(19).…”

Section: Discussionmentioning

confidence: 99%

Hyperalgesic effect induced by barbiturates, midazolam and ethanol: pharmacological evidence for GABA-A receptor involvement

Tatsuo

Yokoro²,

Salgado³

et al. 1997

Braz J Med Biol Res

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The involvement of GABA-A receptors in the control of nociception was studied using the tail-flick test in rats. Non-hypnotic doses of the barbiturates phenobarbital (5-50 mg/kg), pentobarbital (17-33 mg/ kg), and thiopental (7.5-30 mg/kg), of the benzodiazepine midazolam (10 mg/kg) or of ethanol (0.4-1.6 g/kg) administered by the systemic route reduced the latency for the tail-flick response, thus inducing a 'hyperalgesic' state in the animals. In contrast, non-convulsant doses of the GABA-A antagonist picrotoxin (0.12-1.0 mg/kg) administered systemically induced an increase in the latency for the tail-flick response, therefore characterizing an 'antinociceptive' state. Previous picrotoxin (0.12 mg/kg) treatment abolished the hyperalgesic state induced by effective doses of the barbiturates, midazolam or ethanol. Since phenobarbital, midazolam and ethanol reproduced the described hyperalgesic effect of GABA-A-specific agonists (muscimol, THIP), which is specifically antagonized by the GABA-A antagonist picrotoxin, our results suggest that GABA-A receptors are tonically involved in the modulation of nociception in the rat central nervous system.

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“…There is sparse evidence for antinociceptive effcts of phenobarbitol in animals, 177 but it has no significant analgesic effects in humans. It was used in conjunction with opioids for sedation 178 , although there is little recent evidence that it is effective.…”

Section: Non-opioid Therapiesmentioning

confidence: 99%

Pain Management in Newborns

Hall¹,

Anand

2014

Clinics in Perinatology

204

126

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Effective pain management is a desirable standard of care for preterm and term newborns and may potentially improve their clinical and neurodevelopmental outcomes. Neonatal pain should be assessed routinely using context-specific, validated and objective pain methods, despite the limitations of currently available tools. Reducing invasive procedures, and using pharmacological, behavioral or environmental measures can be used to manage neonatal pain. Non-pharmacologic approaches include kangaroo care, facilitated tucking, non-nutritive sucking, sucrose and other sweeteners, massage and acupuncture therapy. They are used for procedures causing acute, transient, or mild pain, or as adjunctive therapy for moderate or severe pain. Local and topical anesthetics can reduce the acute pain caused by skin-breaking or mucosa-injuring procedures. Opioids form the mainstay for treatment of severe pain; morphine and fentanyl are the most commonly used drugs, although other opioids are also available. Non-opioid drugs include various sedatives and anesthetic agents, mostly used as adjunctive therapy in ventilated neonates. Acetaminophen, ibuprofen and other drugs are used for neonates, although their efficacy and safety remains unproven. Approaches for implementing an effective pain management program in the Neonatal ICU are summarized, together with practical protocols for procedural, postoperative, and mechanical ventilation-associated neonatal pain and stress.

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Antinociceptive Effects of Phenobarbital in ???Tail-Flick??? Test and Deafferentation Pain

Cited by 9 publications

References 0 publications

Acute phenobarbital administration induces hyperalgesia: pharmacological evidence for the involvement of supraspinal GABA-A receptors

Acute phenobarbital administration induces hyperalgesia: pharmacological evidence for the involvement of supraspinal GABA-A receptors

Hyperalgesic effect induced by barbiturates, midazolam and ethanol: pharmacological evidence for GABA-A receptor involvement

Pain Management in Newborns

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