Analgesic Effect of Ethyl Alcohol

Mu, James; Duthie, A. M.; Duffy, Brian L.; Mckeag, A. M.; Rice, Christopher

doi:10.1093/bja/50.2.139

Cited by 44 publications

(21 citation statements)

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“…The results of this study confirm previous reports (Wolff et al 1941(Wolff et al , 1942James et a/. 1978) of the analgesic efficacy of ethanol.…”

Section: Discussionsupporting

confidence: 93%

“…In the morphine experiment, subjects received a loading dose of 0.2 mg/kg followed by a pharmacokinetically predicted steady state infusion of 0.004 mg/kg per min. This ethanol level was chosen as it has been shown to produce submaximal analgesic effects, with a level of analgesia similar to that of morphine (0.2 mg/kg; James et al 1978). In order to verify the accuracy of the predictions, the ethanol content of expired air was assayed using a Smith and Wesson 'Breathalyser' Model 1OOO.…”

Section: Methodsmentioning

confidence: 99%

“…It has been established that ethanol possesses analgesic properties (Wolff et al 1941(Wolff et al , 1942 and that this analgesia is similar to that of morphine for applied somatic pain (James et al 1978). In view of the similarity of the analgesic effects of the two drugs, it has been suggested that the two drugs act through similar pathways (Eidelberg 1977) and recent reports that intoxication with ethyl alcohol can be reversed by naloxone (Mackenzie 1979; Jeffcoate et al 1979;Lyon & Anthony 1982) might be considered to support this concept.…”

Section: Introductionmentioning

confidence: 99%

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Naloxone Does Not Reverse Ethanol Analgesia in Man

Saddler¹,

Mu²,

Harington³

1985

Clin Exp Pharma Physio

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The effects of intravenously administered ethanol and morphine on pain threshold, reaction time, motor skills and short-term memory were investigated, and the ability of naloxone to reverse any changes was studied. Morphine (loading dose 0.2 mg/kg with an infusion of 0.004 mg/kg per min) and ethanol (loading dose 0.75 ml/kg with an infusion of 0.0025 ml/kg per min) produced a similar increase in pain threshold of 6.3 (s.e.m. = 1.5, n = 8) pain units and 7.7 (s.e.m. = 1.9, n = 8) pain units, respectively. Naloxone 0.015 mg/kg produced a significant reduction in pain threshold in the morphine group, but not in the ethanol group, and there was a significant difference between the groups following naloxone (P less than 0.05, t-test, 7 d.f.). Ethanol produced a significantly greater deterioration in motor skills than did morphine (P less than 0.05, t-test, 7 d.f.) and performance in both groups was improved following naloxone (P less than 0.05, t-test, 7 d.f.). There was no significant change in the other modalities studied. It is concluded that the reversal of ethanol effects by naloxone is probably due to a non-specific analeptic action rather than blockade of opioid receptors.

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“…The results of this study confirm previous reports (Wolff et al 1941(Wolff et al , 1942James et a/. 1978) of the analgesic efficacy of ethanol.…”

Section: Discussionsupporting

confidence: 93%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Naloxone Does Not Reverse Ethanol Analgesia in Man

Saddler¹,

Mu²,

Harington³

1985

Clin Exp Pharma Physio

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“…Ethanol at clinically relevant concentrations, shortens AP, prolongs refractory period and decreases firing frequency in a subgroup of primary afferent neurons, most likely nociceptors, by activation of BK K (Ca) channels [27]. Thus, modulation of sensory information in primary afferent neurons may explain partly the analgesic and anesthetic effect of ethanol [43,95]. Similarly, the anesthetic and analgesic effects of chloral hydrate can be partly explained by the 20-fold more potent than ethanol activating effect of its active metabolite 2,2,2-trichloroethanol (TCE) on BK channels of DRG neurons, which results in a significant outward current and AP shortening with subsequent excitability reduction [26].…”

Section: Discussionmentioning

confidence: 99%

Opposing effects of spinal nerve ligation on calcium-activated potassium currents in axotomized and adjacent mammalian primary afferent neurons

Sarantopoulos¹,

McCallum²,

Rigaud³

et al. 2007

Brain Research

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Calcium-activated potassium channels regulate AHP and excitability in neurons. Since we have previously shown that axotomy decreases I Ca in DRG neurons, we investigated the association between I Ca and K (Ca) currents in control medium-sized (30-39 μM) neurons, as well as axotomized L5 or adjacent L4 DRG neurons from hyperalgesic rats following L5 SNL. Currents in response to AP waveform voltage commands were recorded first in Tyrode's solution and sequentially after: 1) blocking Na + current with NMDG and TTX; 2) addition of K (Ca) blockers with a combination of apamin 1μM, iberiotoxin 200 nM, and clotrimazole 500 nM; 3) blocking remaining K + current with the addition of 4-AP, TEA-Cl, and glibenclamide; and 4) blocking I Ca with cadmium. In separate experiments, currents were evoked (HP −60 mV, 200 ms square command pulses from −100 to +50 mV) while ensuring high levels of activation of I K(Ca) by clamping cytosolic Ca 2+ concentration with pipette solution in which Ca 2+ was buffered to1μM. This revealed I K(Ca) with components sensitive to apamin, clotrimazole and iberiotoxin. SNL decreases total I K(Ca) in axotomized (L5) neurons, but increases total I K(Ca) in adjacent (L4) DRG neurons. All I K(Ca) subtypes are decreased by axotomy, but iberiotoxin-sensitive and clotrimazole-sensitive current densities are increased in adjacent L4 neurons after SNL. In an additional set of experiments we found that small sized control DRG neurons also expressed iberiotoxin-sensitive currents, which are reduced in both axotomized (L5) and adjacent (L4) neurons.Conclusions: Axotomy decreases I K(Ca) due to a direct effect on K (Ca) channels. Axotomy-induced loss of I Ca may further potentiate current reduction. This reduction in I K(Ca) may contribute to elevated excitability after axotomy. Adjacent neurons (L4 after SNL) exhibit increased I K(Ca) current.

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“…Most tools and tactics generally available to LEP work from the perspective of inducing compliance through painful stimulus, such as impact batons, pepper spray, or hand-to-hand combat. Sometimes these tools and tactics are ineffective because the subject has a decreased perception of pain from conditions such as excited delirium or alcohol intoxication (16,17). The condition of excited delirium seems to occur simultaneously with significant metabolic acidosis, and death has occurred in association with this condition (16).…”

Section: Discussionmentioning

confidence: 99%