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Biomedical subjects

F S Messiha

Publications and source records attributed to F S Messiha.

At least 109 records · Page 6Linked to original sources
PubMed1979

Cyclobenzaprine and ethanol interaction.

The effects of cyclobenzaprine, a tricyclic compound, on the central depressant action of ethanol and on hepatic ethanol metabolizing enzymes were studied in rodents. Administration of cyclobenzaprine, 5 mg/kg, IP, 30 min prior to a narcotic dose of ethanol solution, 5 g/kg, IP, enhanced ethanol-produced narcosis in mice. This effect was greater in male than in female mice. Cyclobenzaprine inhibited endogenous rat liver alcohol dehydrogenase in vitro in the concentration range between 10(-5) M and 10(-6)M. Cyclobenzaprine exerted little effect on hepatic aldehyde dehydrogenase in vitro. The results suggest that cyclobenzaprine possesses depressant properties and inhibition of liver alcohol dehydrogenase may underlie the observed behavioral response studied. It is concluded that alteration of endogenous liver alcohol dehydrogenase by certain tricyclic antidepressant drugs may be involved in the mechanism(s) of their toxic interaction with ethanol.

Alcohol Oxidoreductases↗
PubMed1978

Cesium and rubidium salts: effects on voluntary intake of ethanol by the rat.

The effects of RbCl and CsCl on voluntary intake of ethanol solution by rats preferring ethanol solution 5% (w/w) over water as the drinking fluid was studied as a function of the dose given and the vehicle injected. Administration of RbCl or CsCl, 0.5 mEq/kg/day or 1.5 mEq/kg/day for three consecutive days, did not alter amounts of ethanol consumed. Repeated administration of RbCl or CsCl, 3.0 mEq/kg/day for three days, produced some moderate reduction in ethanol consumption. Simultaneous injection of RbCl (1.5 mEq/kg) and CsCl (1.5 mEq/kg) resulted in greater and profound lasting decrease in ethanol drinking. The later treatment did not alter specific activities of rat liver alcohol- and aldehyde dehydrogenase from saline treated controls. In general, dissolving the chloride salt of the alkali metals in saline resulted in greater effects on ethanol drinking than that determined after identical dose injected with water as the vehicle. The possible mechanism(s) underlying the effects of alkali metal salts used are suggested.

Alcohol Drinking↗
PubMed1978

Voluntary drinking of ethanol by the rat: biogenic amines and possible underlying mechanism.

The present study evaluates the possible relationship between certain biogenic amine metabolites-produced changes in voluntary drinking of ethyl alcohol (ET) solution by the rat and their in vivo effects on the enzymes primarily involved in the hepatic metabolism of ET, i.e., liver alcohol-(L-ADH) and aldehyde dehydrogenase (L-ALDH). In experiments on voluntary intake of ET solution by the rat, compounds selected were injected, 0.5 mM/kg, IP. Administration of vanillylmandelic acid (VMA) and 5-hydroxyindoleacetic acid (5HIAA) and homovanillic acid (HVA) markedly reduced ET drinking. Similar significant effects were seen after administration of the neutral metabolites of the biogenic amines tested, after injection of metanephrine or 3-methoxy-4-hydroxyphenylpyruvic acid. Threodihydroxyphenylserine but not L-dopa reduced ET intake by the rat. Treatment with peripheral decarboxylase inhibitors, i.e., carbidopa, 50 mg/kg, IP, significantly reduced ET drinking as contrasted with nonsignificant decline in ET consumption following benserazide, 500 mg/kg, IP. In the biochemical study, short-term administration of the compounds selected produced varied effects on L-ADH and L-ADH. It is suggested that alteration of hepatic ADH by the compounds tested might account for the observation reduced ET drinking thereby, indicating the contribution of peripheral sources rather than central factors in mediating the behavioral effects studied.

Alcohol Drinking↗
PubMed1978

Antagonism of ethanol-evoked responses by amantadine: a possible clinical application.

The behavioral and biochemical effects of amantadine hydrochloride (ATD) on some ethanol (ETOH) mediated responses in rats and mice were studied. Administration of ATD, 0.5 mM/kg IP, prior to a narcotic dose of ETOH significantly decreased the central depressant action of ETOH, as measured by the duration of ETOH-produced narcosis in mice. The time required for the onset of ETOH-narcosis was significantly delayed in ATD-treated mice compared to controls. Analyses of whole blood and brain ETOH concentrations showed that ATD-treatment prior to ETOH significantly reduced brain content of ETOH from saline-pretreated mice at the time of onset of ETOH narcosis as well as 30 min after ETOH injection without concomitant change in blood ETOH concentrations at the respective time intervals. Administration of ATD 0.5mM/kg IP, reduced voluntary intake of ETOH by rats voluntarily selecting 5% ETOH solution over water as the drinking fluid. There were no changes in cytoplasmic rat liver alcohol dehydrogenase (L-ADH) and mitochondrial aldehyde dehydrogenase (L-ALDH) activities in rats maintained on water or 5% ETOH as the drinking fluid and administered ATD, 0.5 mM/kg IP, once or identical dose once daily for six consecutive days. However, ATD produced in vitro non-competitive inhibiton of both L-ADH and L-ALDH at a concentration range between 10(-3) M and 3 x 10(-3) M assay mixture. The results indicate the potency of ATD in negating ETOH-mediated responses measured and suggest for a possible clinical trial for ATD in the management of alcoholic patients provided it is devoid of disulfiram-like reaction in man.

Alcohol Drinking↗
PubMed1978

Anti-depressant action of caesium chloride and its modification of chlorpromazine toxicity in mice.

1. Adult male mice were treated with caesium chloride (1.0 mEq/kg, i.p.) once daily for 54 consecutive days before administration of a single dose or reserpine (2.0 mg/kg) or (+)-amphetamine (1.0 mg/kg). Pretreatment with caesium chloride resulted in potentiation of amphetamine-produced enhancement of motility and in antagonism of reserpine-induced behavioural depression in mice as measured by a locomotor activity test, compared to the respective controls. 2. Chronic administration of caesium chloride (1.0 mEq/kg daily) with gradual dose build-up of chlorpromazine (up to 50 mg kg-1 day-1) counteracted chlorpromazine-produced mortality in mice. 3. The results suggest an antidepressant property of Cs+ and the combined treatment of caesium chloride with chlorpromazine might have a clinical application, i.e. in the management of chlorpromazine-induced adverse reaction.

Animals↗