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PubMed1978

Experimental barbiturate dependence. I. Barbiturate dependence development in rats by drug-admixed food (DAF) method.

A method for testing a rat's physical-dependence liability to sedaditive-hypnotic agents and for evaluating that dependence was studied by using the method. Rats received phenobarbital- or barbital-admixed food on a graded-increase dosage schedule over 30-40 days. Manifestations of CNS-suppressing action of either drug (e.g., systemic muscle relaxation, motor incoordination, staggering gait, and ptosis) persisted day and night during the drug medication. Twenty-four to 48 h after withdrawal of either drug, abstinence symptoms (e.g., muscle fasciculation, nuchal twitching, vocalization, increased irritability, ataxia, hyperthermia, and clonic-tonic and grand mal-type convulsions) were evidenced in all animals (N = 6), some of which died after convulsions. These withdrawal signs in rats were classified and found to be closely correlated with the magnitude of weight loss during the withdrawal. The calssification provides a basis for quantitatively assessing physical-dependence liability. The data obtained in the present study suggest that rats, like dogs and monkeys, are suitable experimental animals for tests in early stages of dependence liability, and that the administration of drug-admixed food is a useful method of developing dependence on both barbiturate and morphine-type drugs.

Animal Feed↗
PubMed1975

Interactions of tricyclic antidepressants and barbiturates in barbiturate-tolerant and nontolerant rats.

Pretreatment of rats with tricyclic antidepressants, imipramine, desipramine, amitriptyline and nortriptyline, at two doses (5 and 25 mg/kg) 20 minutes before administration of barbiturate markedly reduced the latent period of the response to barbital and prolonged the sleeping time induced by pentobarbital (PB) and barbital. The effects were dose-dependent. The prolonged sleeping time produced by PB was associated with decreases in the rates of disappearance of PB from the brain and plasma. The effect of tricyclic antidepressants on PB hypnosis in PB-tolerant and nontolerant rats was apparently not related to change in central nervous system (CNS) sensitivity to PB, since at the time of awakening there were no significant differences in the concentrations of unmetabolized PB in either the plasma or brain of tricyclic antidepressant-treated animals as compared to controls. As barbital is not metabolized, potentiation of barbital hypnosis by tricyclic antidepressants must be attributable to a direct effect on CNS rather than on liver microsomal enzymes. Direct evidence was provided by the findings that amitriptyline accelerated the brain uptake of barbital and that amitriptyline-treated animals lost and recovered the righting reflex at brain barbital levels lower than those of controls. Rats made tolerant to the hypnotic effect of barbital also became tolerant, in varying degrees, to the hyposis-prolonging properties of tricyclic antidepressants. It is concluded that tricyclic antidepressants prolong PB sleeping time in PB-tolerant and nontolerant rats by inhibiting its biotransformation in the liver. The action of tricyclic antidepressants to prolong the hypnotic action of barbital in normal rats is related to their direct effects on CNS sensitivity to barbital, but such effects are makedly diminished after animals become tolerant to barbital.

Amitriptyline↗
PubMed1988

Photochemical degradation of barbituric acid derivatives. Part 8: Photolysis of sodium salts of barbiturates in solid state.

After the UV irradiation of suspensions of barbiturate sodium salts in paraffin oil the IR spectra revealed two IR absorption bands at ca. 2170 and 2250 cm-1. The effects of different conditions of the photochemical process and the addition of nucleophilic reagents after irradiation on the intensity of these bands were studied. The origin of 2170 cm-1 band was interpreted in terms of the isocyanate intermediate which is formed after the pyrimidine ring opening.

Barbiturates↗
PubMed1982

Prolongation of barbiturate-induced sleeping time in mice by dimethylformamide (DMF) and other non-polar solvents: absence of an effect on hepatic barbiturate-metabolising enzymes.

Prior administration of non-polar solvents was shown to prolong sleeping time in female mice induced with pentobarbitone sodium (37.5 mg/kg). The doses of solvents to double sleeping time were extrapolated from individual dose-response curves: they were (g/kg i.p.): dimethylformamide (DMF) 1.15: polyethyleneglycol 2.0: glycerol 0.66: dimethylsulphoxide 1.78: and sulpholone 1.26. The prolongation of sleeping time with DMF was not due to inhibition of hepatic microsomal enzymes because mice pretreated with SK & F 525A (40 mg/kg i.p.) did not exhibit a much greater solvent-induced effect than occurred in control (unpretreated) mice. DMF prolonged sleeping time in mice injected with thiopentone sodium (37.5 mg/kg i.v.), a drug known not to have its duration of narcotic effect determined by microsomal enzyme metabolism. It is concluded that prolongation of barbiturate-induced sleeping time in mice by DMF is not due to an inhibitory effect of the solvent on the hepatic microsomal enzymes.

Animals↗