Amobarbital
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A sedative and hypnotic barbiturate first discovered in 1923. Formerly widely used recreationally and medically, barbiturates have declined in popularity with the appearance of benzodiazepines and other drugs with less serious consequences in overdose.TS
Oral
Route dataTripSit
| Threshold | Light | Common | Strong | Heavy |
|---|---|---|---|---|
| — | — | 50–75 mg | 75–150 mg | —+ |
| Onset | 10–30 minutes |
|---|---|
| Total | 5–9 hours |
| After-effects | 2–12 hours |
Mechanism of actionPH
Amobarbital (like all barbiturates) works by binding to the GABAA receptor at either the alpha or the beta sub unit. These are binding sites that are distinct from GABA itself and also distinct from the benzodiazepine binding site. Like benzodiazepines, barbiturates potentiate the effect of GABA at this receptor. This GABAA receptor binding decreases input resistance, depresses burst and tonic firing, especially in ventrobasal and intralaminar neurons, while at the same time increasing burst duration and mean conductance at individual chloride channels; this increases both the amplitude and decay time of inhibitory postsynaptic currents. In addition to this GABA-ergic effect, barbiturates also block the AMPA receptor, a subtype of glutamate receptor. Glutamate is the principal excitatory neurotransmitter in the mammalian CNS. Amobarbital also appears to bind neuronal nicotinic acetylcholine receptors.
The exact mechanism(s) by which barbiturates exert their effect on the CNS, has not been fully elucidated. However, it is believed that such effects are related, at least partially, to the drugs' ability to enhance the activity of gamma-aminobutyric acid (GABA), the principal inhibitory neurotransmitter in the CNS, by altering inhibitory synaptic transmissions that are mediated by GABAA receptors. /Barbiturates General Statement/
Although the drugs act throughout the CNS, a site of particular sensitivity is the polysynaptic midbrain reticular formation which is concerned with the arousal mechanism. Barbiturates induce an imbalance in central inhibitory and facilitatory mechanisms influencing the cerebral cortex and the reticular formation. The significance of the effect of barbiturates on neurotransmitters is unclear. It appears that the drugs decrease the excitability of both presynaptic and postsynaptic membranes. It has not been determined which of the various actions of barbiturates at cellular and synaptic levels are responsible for their sedative and hypnotic effects. /Barbiturates General Statement/
Relatively low doses of the barbiturates depress the sensory cortex, decrease motor activity, and produce sedation and drowsiness. In some patients, however, drowsiness may be preceded by a period of transient elation, confusion, euphoria, or excitement, especially after subhypnotic doses of aprobarbital, pentobarbital, or secobarbital. /Barbiturates General Statement/
Larger doses distort judgment, cloud perception, suppress motor activity, and produce drowsiness and sleep. Still larger doses induce anesthesia. Barbiturate-induced sleep differs from physiologic sleep. Barbiturates reduce the rapid eye movement (REM) or dreaming stage of sleep. Stages III and IV sleep are also decreased. Although tolerance develops to the REM-suppressant effects during chronic administration, REM rebound occurs when the drugs are withdrawn, and the patient may experience markedly increased dreaming, nightmares, and/or insomnia. /Barbiturates General Statement/
For more Mechanism of Action (Complete) data for Amobarbital (18 total), please visit the HSDB record page.
Pharmacokinetics
Half-lifePH
Following bolus iv administration, plasma concentrations of amobarbital decline in a biphasic manner with a half-life of about 40 minutes for the first phase and 20-25 hours for the second phase, although the second phase half-life has ranged from 14-42 hours in individual patients.
The half-life of amobarbital was investigated in 36 unrelated subjects; half-life (23.8 hr) appeared to be normally distributed.
Following im injection of amylobarbitone sodium 200 mg to mildly hypertensive women in labor 0.7 to 3.5 hr before delivery, the plasma-half-life of amylobarbitone was 2.5 times as long in the neonates as in the mothers. /Amobarbital sodium/
AbsorptionPH
Following oral or rectal admin, the onset of action varies from 10-30 min for ... amobarbital ... Following iv admin of the sodium salts of ... amobarbital, the onset of action ranges from almost immediately for pentobarbital ... .
About 40 to 60% of amylobarbitone is bound to plasma proteins.
Following admin of radioactively labelled amylobarbitone to 2 healthy subjects 79 to 92% was recovered in urine in 6 days and only 4 to 5% in the feces. Unchanged drug was practically absent from both urine and feces.
Fluid & tissue specimens collected from 30 subjects at autopsy were assayed for amylobarbitone (amobarbital), butobarbitone (butethal), pentobarbitone (pentobarbital), quinalbarbitone (secobarbital) and the corresponding hydroxylated metabolites by GLC. Where one barbiturate was ingested, an inverse relationship between lipid solubility of the drug and the distribution in fluids and tissues was observed. In most cases the liver, and in the remainder the spleen, contained the highest concn of barbiturate. Bile concn were often in excess of those in the corresponding liver. The metabolites of the 4 sedative barbiturates were usually present in lower amounts than the parent drugs in the fluids and tissues of most subjects, but urine often contained much higher concn of metabolites, sometimes exceeding that of the parent drug in the liver. Admin of 2 or more barbiturates together did not appear to affect the distribution and metabolism of the individual drugs.
For more Absorption, Distribution and Excretion (Complete) data for Amobarbital (17 total), please visit the HSDB record page.
MetabolismPH
Amobarbital is metabolized by the liver via penultimate oxidation of the 3-methylbutyl substituent to form a tertiary alcohol, hydroxyamobarbital, which is an inactive metabolite. About 40-50% of an oral hypnotic dose of amobarbital is excreted in urine as hydroxyamobarbital and its glucuronide conjugates. Less than 1% of an oral hypnotic dose of the drug is excreted in urine unchanged. Conjugates of hydroxyamobarbital excreted in feces or urine and/or further oxidation products not yet identified may account for the remainder of the dose.
Following admin of radioactively labelled amylobarbitone to two healthy subjects ... less than 50% of the dose was identified as 3'-hydroxyamylobarbitone. A second main metabolite was identified as N-hydroxyamylobarbitone and was found to account for up to 30% of the dose.
Relative proportion of amobarbital metabolites in urine is highly variable and observations of plasma half-life give no indication of this variability. A valid estimate of a given person's metabolite pattern can be obtained by studying single urine specimen in postdistributive phase. Two metabolites were measured in urine specimen in the postdistributive phase. The 2 metabolites were 3'-hydroxyamobarbital as product of side chain hydroxylation and N-beta-d-glycopyranosyl amobarbital, a glucose conjugate.
N-Hydroxyamylobarbitone was synthesized and its occurrence as a urinary metabolite was studied in 13 subjects taking 200 mg sodium amobarbital. It was concluded that the excretion of free N-hydroxyamylobarbitone is not significant in the metabolism of amobarbital sodium. /Amobarbital sodium/
For more Metabolism/Metabolites (Complete) data for Amobarbital (8 total), please visit the HSDB record page.
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