Toxic interactions of ethanol with other central depressants: Antagonism by naloxone to narcosis and lethality

  title={Toxic interactions of ethanol with other central depressants: Antagonism by naloxone to narcosis and lethality},
  author={Andrew K. S. Ho and Chiu C. Ho},
  journal={Pharmacology Biochemistry and Behavior},
  • A. Ho, C. Ho
  • Published 1 July 1979
  • Medicine, Chemistry
  • Pharmacology Biochemistry and Behavior
The effects of naloxone on narcosis and/or lethality induced by diazepam, lithium, methaqualone and phenobarbital either alone or in combination with ethanol were studied in mice. Interaction toxicities between ethanol and the various psychotropic drugs were dose-dependent and so was the degree of antagonism by naloxone. Treatment with phenobarbital (10 mg/kg) or methaqualone (50 mg/kg) or lithium (4 meq/kg) prolonged the narcosis induced by ethanol (5 g/kg) by 45, 269 and 107% respectively… 
Differential effects of TRH, amphetamine, naloxone, and fenmetozole on ethanol actions: attenuation of the effects of punishment and impairment of aerial righting reflex.
The inconsistent pattern of "antagonist" interactions of these drugs with the behavioral actions of ethanol suggests that ethanol alters several neurochemical systems to produce its behavioral effects.
The effects of opiate antagonists on the discriminative stimulus properties of ethanol
It is demonstrated that the discriminative stimulus properties of ethanol do not require intact opiate pathways, which implies that the neuropharmacological mechanisms mediating ethanol's stimulus properties in rodents are different from the mechanismsmediating many other behavioral actions of ethanol, including its reinforcing properties.
Interactions between naltrexone and non-opiate drugs evaluated by schedule-controlled behavior
Seven non-opiate drugs were studied, alone and in conjunction with naltrexone, in rats responding under a multiple fixed-interval 5-min, fixed-ratio 30-response schedule of food presentation to study the effects of narcotic antagonists on dopaminergic systems.
Effects of naloxone and buprenorphine on intravenous acetaldehyde self-injection in rats
The findings are consistent with the hypothesis of opiate involvement in acetaldehyde self-administration, but caution must be exercised when drawing conclusions about the participation of endogenous opiates inacetaldehyde-mediated behavior.
  • M. Kreek
  • Medicine
    Annals of the New York Academy of Sciences
  • 1981
Clinical studies in patients on chronic steady-dose methadone maintenance treatment, without liver disease, polydrug abuse, or heavy use of ethanol, show no significant dispositional interactions between methad one and disulfiram (Antabuse) when the latter was given for one week for study purposes only.
Genetic differences in opiate receptor concentration and sensitivity to ethanol's effects
The hypothesis that genetic differences in opiate receptor concentration are involved in determining the sensitivity to some of the effects of alcohol was studied and it is suggested that the hypothermic and analgesic effects of ethanol are at least partly mediated by opiate receptors and are correlated with genetic differences.
Naloxone antagonizes ethanol- but not α-hydroxybutyrate-induced sleep in mice
Abstract The present study examined the effect of naloxone on ethanol- and γ-hydroxybutyric acid-induced narcosis in mice and the changes induced by these drugs on striatal dopamine metabolism. The
Naloxone has no effect on ethanol-induced impairment of psychomotor performance in man
There was no suggestion of ethanol impairment being moderated by naloxone, whether it was given before or after ethanol, and there were no significant differences in either blood or breath ethanol concentrations at any time between the ethanol + naloxin and ethanol + saline groups in either Experiment 1 or 2.
Effects of naloxone on ethanol dependence in rats.
It is indicated that naloxone can alter the effects of chronic ethanol exposure and further suggest that ethanol may exert some of its actions via the brain opioid system.
Effects of ethanol and naltrexone on free-operant avoidance behavior in rats
The results provided little support for the hypothesis that the effects of ethanol on avoidance performance are mediated by the opiate receptor system, and instead provided evidence of heightened sensitivity to ethanol.


Interaction toxicity between ethanol and narcotics in mice with reference to alpha-l-acetylmethadol (LAAM)
Toxicity with the combined administration of LAAM and ethanol was attributed in part to the retention of ethanol, whereas naloxone and dextrorphan, an inactive stereoisomer of levorphanol, produced a small but significant increase.
The influence of naloxone on barbiturate anesthesia and toxicity in the rat.
The findings of this study indicate that therapeutic trials with relatively large doses of naloxone are justifiable in patients intoxicated with barbiturates.
The human pharmacology and abuse potential of N-allylnoroxymorphone (naloxone).
It is concluded that naloxone does not have abuse potential of the morphine type since it does not produce subjective effects or physical dependence and precipitates abstinence in morphine-dependent subjects.
Alkali metal ions and ethanol narcosis in mice.
It is concluded that both Rb+ and Cs+ possess antidepressant properties and might be useful agents in negating the depressant action of ETOH and/or some of its toxic manifestations.
Analeptic and antianaleptic effects of naloxone and naltrexone in rabbits.
Abstract Naloxone (5 mg/kg), but not naltrexone, shortened the duration of anaesthesia in rabbits pretreated with pentobarbital. This analeptic effect was blocked by atropine, but not by
Naloxone-induced inhibition of ethanol dependence in mice
The demonstration of an effect on opiate activity by certain neuroamine-derived TIQs prompted us to investigate the question further, and it was interesting to know the effect of naloxone, an agent known to block the development of dependence to opiates, on theDevelopment of dependence on ethanol.
Antagonism of general anesthesia by naloxone in the rat.
The EEG patterns of several animals anesthetized with either cyclopropane or halothane changed to patterns consistent with lighter planes of anesthesia after naloxone administration, suggesting that anesthetics may release an endogenous morphine-like factor in the central nervous system.
Naloxone as a GABA antagonist: evidence from iontophoretic, receptor binding and convulsant studies.
Naloxone displaced 3H-GABA from receptor sites in rate forebrain and cerebellum, with similar low potency, and Diazepam, which protects mice against convulsions elicited by bicuculline, but not by strychnine, also protected mice against nalox one.
Potentiation of lithium toxicity by ethanol in rats and mice.
  • A. Ho, C. C. Ho
  • Chemistry, Medicine
    Alcoholism, clinical and experimental research
  • 1978
Retention of lithium induced by ethanol appeared to be responsible for the potentiation of lithium toxicity and the potential hazard in the interaction between lithium and ethanol is discussed.
Ethanol: modifications of acute intoxication by divalent cations.
The results suggest the existence of a central calcium pool that is involved in ethanol intoxication in rodents and the effects of cations on ethanol-induced hypothermia were less significant.