Analgesic Effect of Ethyl Alcohol

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

doi:10.1097/00132586-197812000-00019

Cited by 6 publications

(8 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…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%

“…There is evidence that ethanol and opiates have biochemical and behavioural mechanisms in common (Blum 1980). 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%

See 2 more Smart Citations

Naloxone Does Not Reverse Ethanol Analgesia in Man

Saddler¹,

Mu²,

Harington³

1985

Clin Exp Pharma Physio

Self Cite

View full text Add to dashboard Cite

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.

show abstract

“…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

Self Cite

View full text Add to dashboard Cite

show abstract

“…Moreover, ethanol has been clinically used as analgesic and anaesthetic (Woodrow and Eltherington, 1988), and yet the systems mediating these effects remain to be fully addressed. A few studies (e.g., James et al., 1978) have reported that these alcohol effects could be, at least, partially attributed to ethanol actions on the peripheral nervous system (PNS).…”

Section: Ethanol Reduces the Excitability Of Sensory Neurons By Activmentioning

confidence: 99%

Ethanol Interactions With Calcium‐Dependent Potassium Channels

Brodie

Scholz

Weiger

et al. 2007

Alcoholism Clin & Exp Res

102

View full text Add to dashboard Cite

In most neurons and other excitable cells, calcium-activated potassium channels of small (SK) and large conductance (BK; MaxiK) control excitability and neurotransmitter release. The spontaneous activity of dopamine neurons of the ventral tegmental area is increased by ethanol. This ethanol excitation is potentiated by selective blockade of SK, indicating that SK channels modulate ethanol stimulation of neurons that are critical in reward and reinforcement. On the other hand, ethanol directly modulates BK channel activity in a variety of systems, including rat neurohypophysial nerve endings, primary sensory dorsal root ganglia, nucleus accumbens neurons, Caenorhabditis elegans type-IV dopaminergic CEP neurons, and nonneuronal preparations, such as rat pituitary cells, cerebrovascular myocytes and human umbilical vein endothelial cells. Ethanol action on BK channels can modify neuropeptide and growth hormone release, nociception, cerebrovascular tone, and endothelial proliferation. Ethanol modulates BK channels even when the drug is evaluated using recombinant BK channel-forming alpha (slo) subunits or channel reconstitution in artificial, binary lipid bilayers, indicating that the slo subunit and its immediate lipid microenvironment are the essential targets of ethanol. Consistent with this, single amino acid slo channel mutants display altered ethanol sensitivity. Furthermore, C. elegans slo1 null mutants are resistant to ethanol-induced motor incoordination. On the other hand, Drosophila melanogaster slo null mutants fail to acquire acute tolerance to ethanol sedation. Ethanol action on slo channels, however, may be tuned by a variety of factors, including posttranslational modification of slo subunits, coexpression of channel accessory subunits, and the lipid microenvironment, resulting in increase, refractoriness, or even decrease in channel activity. In brief, both SK and BK channels are important targets of ethanol throughout the body, and interference with ethanol effects on these channels could form the basis for novel pharmacotherapies to ameliorate the actions or consequences of alcohol abuse.

show abstract

“…As such, our current understanding of alcohol analgesia is limited. This is perhaps surprising considering the long-standing acceptance of the analgesic properties of alcohol and claims of an analgesic potency comparable to opiates 36,69 . Given the general use of small samples and variability in dosages, administration methods and outcome measures in previous studies 34 We therefore conducted a meta-analysis of controlled experiments examining the impact of measured alcohol dosages vs. no-alcohol on response to noxious stimulation in human participants to determine the: (1) the existence of alcohol analgesia; (2) the magnitude of any analgesic effects; and (3) the impact of moderating variables.…”

Section: Introductionmentioning

confidence: 99%