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PubMed1989

Comparative study on barbiturates using isolated single neurons: GABA-mimetic action and augmentatory action on GABA response.

The comparisons among barbiturate derivatives in both GABA-mimetic action and augmentatory effect on GABA response were made. Experiments were performed on single neurones isolated from frog dorsal root ganglia, using a concentration clamp technique which combines a suction pipette technique (internal perfusion and voltage-clamp) with a rapid external solution exchange within 2 ms. Barbiturates employed here were secobarbital, pentobarbital, hexobarbital and phenobarbital. All barbiturates at the concentrations over 1 x 10(-4) M evoked the chloride current (ICl) dose-dependently. In the GABA-mimetic action of barbiturates the potency was in the order of secobarbital greater than pentobarbital greater than hexobarbital greater than phenobarbital. All barbiturates at the concentrations over 1 x 10(-6) M (but up to 1 x 10(-3) M) augmented the GABA-induced ICl. Potency order of barbiturates in augmenting GABA response was the same as that in their GABA-mimetic actions when the concentration was 1 x 10(-4) M or less. However at the concentration of 1 x 10(-3) M the efficacies of secobarbital and pentobarbital in augmenting GABA response were greatly reduced while the other two barbiturates produced further augmentation.

Animals↗
PubMed1983

Long-lasting effects of early barbiturates on central nervous system and behavior.

Forty years of prescribing barbiturates to pregnant women and infants, and thirty years of animal research have shown that barbiturates affect the developing central nervous system (CNS) and behavior. This paper compiles and reviews animal and selected human literature in this research area. Early barbiturate exposure in animals reduces brain weight with related changes in brain biochemistry and neuromorphology. Significant changes may be found in surviving adult offspring. Evidence of CNS and behavioral damage in human beings due to early barbiturate exposure is not clearcut, however, confounded by the conditions for which the drugs are prescribed. In animals, early drug exposure significantly reduces levels of hormones, vitamins, and other biologically active macromolecules via (long-lasting) induction of hepatic metabolizing enzymes. Whether or not in humans treated with barbiturates, hormone levels remain within the normal range (by-feed-back regulation) and, also, if vitamin deficiencies can be simply corrected by supplements is still being debated. Early barbiturates administered to animals is associated with long-lasting disturbances in activity, learning performance, sexual behavior, and reproductive function, but not in a simple dose-exposure related manner. Animal studies show that long-lasting functional tolerance to drugs develops following early barbiturate exposure. Although infants become "passively addicted" following in utero exposure, there is as yet no data on subsequent development of human adult tolerance. Drug related damage must, in any case, be weighed against therapeutic benefits of drug administration and the results of failure to treat.

Animals↗
PubMed1989

Complications associated with barbiturate therapy.

Fifty-six patients with elevated intracranial pressure caused by cerebrovascular accident, head injury, etc., were the subjects of this study. They were divided into three groups: low dose barbiturate therapy (15 patients), high dose barbiturate therapy (24 patients), and control group (17 patients). Barbiturate therapy was instituted using thiamylal, and the complications caused by barbiturate therapy were recorded. In the control group, complications occurred in the liver of two patients, but there were no renal or pulmonary complications. Pulmonary, renal, and hepatic complications were common in the barbiturate groups. Complications in the high dose therapy group were significantly more common than in the control group. Opportunistic infections occurred in ten patients, with seven patients having pneumonia. Only one patient, with pneumonia, was seen in the control group. The deaths of three patients were influenced by complications associated with barbiturate therapy, while the single death in the control group was not associated with the complication of barbiturate therapy.

Adolescent↗
PubMed1997

Determination of barbiturates by solid-phase microextraction (SPME) and ion trap gas chromatography-mass spectrometry.

Solid-phase microextraction (SPME) in conjunction with quadrupole ion trap GC-MS was applied to the determination of a series of barbiturates. A 65 microns Carbowax-divinylbenzene (DVB) SPME fiber was used to successfully extract a series of eight barbiturates from aqueous solution. Absorption kinetics and distribution coefficients for the 65 microns Carbowax-DVB SPME fiber were determined for the compounds. In addition the method was evaluated with respect to linearity, limit of detection, precision, desorption time, and the effect of salt. Limits of detection reached 1 ng/ml for the barbiturates. Linearity was established for the barbiturates over a concentration range of 10-1000 ng/ml, with coefficients of correlation 0.99. Overall, the precision of the method fell between 2.2%-6.5%, depending on the barbiturate. SPME was applied to the identification and quantitation of the barbiturates in a urine matrix. The method was validated by analyzing a reference standard pentobarbital-spiked urine sample. Both standard addition and internal standard with [2H5]-pentobarbital techniques were evaluated, with recoveries found to be 93% and 104%, respectively SPME was then used to rapidly screen a urine specimen tested positive for barbiturates, and butalbital was detected and quantified.

Absorption↗
PubMed1996

Chimeric GABAA/glycine receptors: expression and barbiturate pharmacology.

GABAA and glycine receptors are close relatives in the "gene superfamily" of ligand-gated ion channels, but have distinctly different pharmacology. For example, barbiturates have two effects on GABAA receptors (GABAA-R): at low micromolar concentrations (2-5 microM), the anesthetic barbiturate methohexital potentiates submaximal chloride current responses to GABA; at higher concentrations (20-50 microM), the barbiturate causes direct gating of the channel in the absence of agonist. Neither of these barbiturate effects is seen on the glycine receptor (Gly-R). In order to study the structural parts of the GABAA-R involved in this barbiturate pharmacology, two unique restriction sites were introduced into the cDNAs encoding the alpha 2 and beta 1 subunits of the human GABAA-R and the alpha 1 subunit of the human gly-R. The first site ('X') corresponded to the C-terminal end of the third transmembrane domain (M3) in each subunit and enabled exchange of C-terminal fragment of approximately 100 amino acids (which includes the large 'cytoplasmic loop' and M4 segment) between GABAA-R and Gly-R subunits. The second site ('S') was approximately 30 amino acids 3'- from the N-terminal end of each subunit and enabled exchange of a small N-terminal fragment between GABAA-R and Gly-R subunits. Several chimeric receptor subunit cDNAs were constructed and the resulting receptors tested for their ability to respond to GABA and glycine and for sensitivity to the barbiturate methohextial (MTX). The results show that neither the large C-terminal fragment nor the smaller N-terminal fragment is associated with the enhancement or direct activation of the GABAA-R by MTX. These results demonstrate the viability of chimeric GABAA/Gly-R and suggest that the method will be suitable for further investigation of the molecular basis of the barbiturate pharmacology of the GABA-R.

Anesthetics, General↗
PubMed2003

Orexinergic neurons and barbiturate anesthesia.

Orexins (OXs) regulate sleep with possible interactions with brain noradrenergic neurons. In addition, noradrenergic activity affects barbiturate anesthesia. As we have also recently reported that OXs selectively evoke norepinephrine release from rat cerebrocortical slices we hypothesized that barbiturate anesthesia may result from of an interaction with central orexinergic systems. To test this hypothesis, we performed a series of in vivo and in vitro studies in rats. In vivo, the effects of i.c.v. OX A, B and SB-334867-A (OX1 receptor antagonist) on pentobarbital, thiopental or phenobarbital-induced anesthesia times (loss of righting reflex) was assessed. In vitro effects of barbiturates and SB-334867-A on OX-evoked norepinephrine release from cerebrocortical slice was examined. In Chinese hamster ovary cells expressing human OX1/OX2 receptors OX A- and B-evoked increases in intracellular Ca2+ were measured with and without barbiturates. OX A and B significantly decreased pentobarbital, thiopental and phenobarbital anesthesia times by 15-40%. SB-334867-A increased thiopental-induced anesthesia time by approximately by 40%, and reversed the decrease produced by OX A. In vitro, all anesthetic barbiturates inhibited OX-evoked norepinephrine release with clinically relevant IC50 values. A GABAA antagonist, bicuculline, did not modify the inhibitory effects of thiopental and the GABAA agonist, muscimol, did not inhibit norepinephrine release. In addition there was no interaction of barbiturates with either OX1 or OX2 receptors. Collectively our data suggest that orexinergic neurons may be an important target for barbiturates, and GABAA, OX1 and OX2 receptors may not be involved in this interaction.

Animals↗
PubMed1985

Barbiturates in brain ischaemia.

This review has indicated that barbiturates are useful in controlling ICP during anaesthesia in patients with intracranial hypertension. While laboratory data indicate that intraoperative administration of barbiturates during episodes of transient cerebral ischaemia, associated with surgical revascularization procedures, should be efficacious, current intraoperative results claiming benefit are anecdotal. Continuous high-dose barbiturate therapy (induced barbiturate coma) for occlusive stroke and persistently increased intracranial pressure is currently undergoing clinical trials. While it is clear that this therapy can often reduce increased ICP in head injured patients, its influence on neurological outcome remains to be determined by a multicentre trial at present in progress. Despite evidence that high-dose barbiturate therapy can reduce the area of infarction in occlusive stroke in the laboratory, organized clinical trials have not yet commenced. Until more definitive knowledge is available concerning the influence of high-dose barbiturate therapy in treating different forms of cerebral ischaemia, its application should be viewed sceptically and limited to centres willing to create an organized data base for inter-institutional evaluation of this form of treatment. If barbiturate therapy proves successful and the mechanisms involved are better understood, drugs with fewer side-effects and risks may become available to combat cerebral ischaemia.

Animals↗
PubMed1996

Inhibition of gap junctional intercellular communication by barbiturates in long-term primary cultured rat hepatocytes is correlated with liver tumour promoting activity.

Rodent liver tumor formation can be promoted by certain barbiturates and this may involve their ability to inhibit hepatocyte gap junctional intercellular communication (GJIC). In order to address the mechanisms and specificity of action of barbiturates on hepatocyte gap junctions, we have compared the effects of liver tumor-promoting barbiturates (phenobarbital, sodium barbital and amobarbital: PB, SB and AB, respectively) and a non-liver tumor-promoting barbiturate (barbituric acid: BA) on primary cultured rat hepatocyte GJIC and connexin32 (Cx32) expression after short (1-24 h) and long (2-14 days) treatment. GJIC was evaluated by fluorescent dye microinjection (dye-coupling); Cx32 expression was monitored by Northern blot, Western blot and immunohistochemistry. Both parameters were maintained at high levels over 14 days by coculture of the cells with WB-F344 rat liver epithelial cells in the presence of dexamethasone. Treatment with PB (2 mM) for 1 h sharply reduced dye-coupling from approximately 90-30%, but the cells fully recovered by 24 h. No inhibition was seen with the other barbiturates over this 1-day treatment period. Longer treatments (2-14 days) with the promoters PB, SB and AB, however, gradually reduced hepatocyte dye-coupling to approximately 30-50%. The non-promoter, BA, did not affect hepatocyte GJIC. These decreases in hepatocyte dye-coupling occurred without changes in Cx32 or gap junction expression. Dye-coupling of WB-F344 cells and expression of their predominant gap junction protein, connexin43 (Cx43), were also not affected. Thus, the inhibition of GJIC was specific to liver tumor promoting barbiturates in hepatocytes, was time-dependent and was not due to altered Cx32 expression.

Animals↗
PubMed2001

In vitro reaction of barbiturates with formaldehyde.

Barbiturates are widely used as sedatives, hypnotics, and antiepileptics, and, when coupled with their narrow therapeutic index, the probability that their use will result in accidental or intentional death is significant. When barbiturates are implicated in a murder or suicide, analysis for their presence is often required. Under certain conditions, barbiturates are quite stable, but conditions found in vivo immediately after death or after embalming may promote barbiturate decomposition. If extensive decomposition occurs, analysis for them may be difficult or impossible. Here, the stability of three representative barbiturates, under conditions that model those likely to prevail in vivo shortly after death and after embalming, have been studied. Solutions of phenobarbital were found to slowly decompose in water over the pH range of approximately 3.5 to 9.5. More rapid decomposition occurred at higher pH, and 2-phenylbutyric acid was the main decomposition product. Formaldehyde (5-20%) accelerated the decomposition rate 3-10-fold such that phenobarbital decomposition could be complete after 30 days. In contrast, pentobarbital decomposed roughly 10 times more slowly and secobarbital did not detectably decompose under any of the conditions studied. Thus, certain barbiturates may partially or completely decompose in vivo after death, especially after embalming, and thus analysis for them may lead to false negatives. However, this work shows that analysis for the parent barbiturate or its predicted decomposition product may provide data that will reduce the likelihood of false negatives.

Barbiturates↗
PubMed1993

Barbiturate action is dependent on the conformational state of the acetylcholine receptor.

BACKGROUND: Barbiturates act on many neuronal ion channels by poorly understood mechanisms. The authors investigated the hypothesis that barbiturates inhibit the transient open-channel conformation of the nicotinic acetylcholine receptor (nAchR) by binding to a discrete site. METHODS: Inhibition curves of the agonist-stimulated efflux of 8bRb+ from nAchR-rich membrane vesicles prepared from the electric tissue of Torpedo nobiliana were obtained for 14 barbiturates using a filter assay. RESULTS: When added simultaneously with agonist, all agents inhibited the ion efflux with half-inhibitory concentrations (IC50), varying from 23 microM for pentobarbital to 880 microM for barbital, and with Hill coefficients of one. The effect of several barbiturates on the agonist concentration-response curve for carbachol-stimulated efflux indicated that this inhibitory action was not competitive. CONCLUSIONS: The IC50s of these agents did not correlate with their octanol/water partition coefficients, nor with general anesthetic potency, although a degree of channel inhibition occurred with many agents at general anesthetic concentrations. The existence of a barbiturate-inhibitory site of action was indicated by the structural specificity. This conclusion was supported by the Hill coefficient of one, and by the high inhibitory potencies, which ruled out membrane perturbations as a mechanism. This site on the transient open-channel conformation exhibits different structure-activity relationships than an allosteric site established by equilibrium barbiturate binding on the resting conformation of the AchR. Thus, barbiturate action depends on the nAchR's conformational state.

Animals↗
PubMed1982

Solubilization by CHAPS detergent of barbiturate-enhanced benzodiazepine-GABA receptor complex.

Barbiturates enhance the binding of [3H]flunitrazepam to benzodiazepine receptors solubilized with the detergent 3-[(3-cholamidopropyl)-dimethylammonio]propanesulfonate (CHAPS) from bovine cortex. The enhancement by the barbiturates is seen as a decrease in the dissociation constant, KD, for specific benzodiazepine binding, with no effect on the number of binding sites. The effect of the barbiturates is facilitated by chloride ions, is concentration-dependent, and has a specificity that correlates well with the anesthetic potency of barbiturates. [3H]Flunitrazepam binding activity is stable with storage at 4 degrees C, but barbiturate enhancement of soluble benzodiazepine binding activity decayed rapidly (t 1/2 = 48 h). [3H]Muscimol binding (GABA receptor) activity was also enhanced by barbiturates. Agarose gel filtration column chromatography of the CHAPS-solubilized receptor proteins showed the same elution profile as receptors solubilized with sodium deoxycholate, and enhancement by barbiturates was observed for both the benzodiazepine and GABA binding activities.

Animals↗
PubMed2004

Inhibition of activator protein 1 by barbiturates is mediated by differential effects on mitogen-activated protein kinases and the small G proteins ras and rac-1.

Barbiturates are known to suppress protective immunity, and their therapeutic use is associated with nosocomial infections. Although barbiturates inhibit T cell proliferation, differentiation, and cytokine synthesis, only thiobarbiturates markedly reduce the activation of immune regulatory transcription factors such as nuclear factor-kappaB and nuclear factor of activated T cells. In this study, we investigated barbiturate-mediated effects on the regulation of the transcription factor activator protein 1 (AP-1) in primary T lymphocytes. We show that both thiobarbiturates and their oxy-analogs inhibit AP-1-dependent gene expression and AP-1 complex formation at clinically relevant doses. Furthermore, mitogen-activated protein (MAP) kinase activity, which transcriptionally and posttranslationally regulates AP-1 complex formation, is suppressed by most barbiturates. CD3/CD28- or phorbol 12-myristate 13-acetate (PMA)/ionomycin-induced p38 and extracellular signal-regulated kinase 1/2 phosphorylation or c-jun NH2-terminal kinase (JNK) 1/2 kinase activity was significantly diminished by pentobarbital, thiamylal, secobarbital, or methohexital treatment. These barbiturates also inhibited the initiators of the MAP kinase cascade, the small G proteins ras and rac-1, and prevented binding to their partners raf-1 and PAK, respectively. Thiopental, unlike the other barbiturates, only reduced ras and JNK activity upon direct CD3/CD28 receptor engagement. Contrarily, upon PMA/ionomycin stimulation, thiopental blocked AP-1-dependent gene expression independently of the small G protein ras and MAP kinases, thus suggesting an additional, unknown mechanism of AP-1 regulation. In conclusion, our results contribute to the explanation of a clinically manifested immune suppression in barbiturate-treated patients and support the idea of a MAP kinase-independent regulation of AP-1 by PKC and calcium in human T cells.

Barbiturates↗
PubMed2003

Effects of barbiturates on human platelet aggregation differ depending on their chemical structures.

The effects of barbiturates on human platelet function are not fully understood. Since we have already revealed the effects and mechanisms of thiopental, thiamylal, and pentobarbital in platelets, the present study attempted to elucidate (i) the effects of other barbiturates on human platelet aggregation, (ii) the underlying mechanisms, and (iii) the structure-function relationship of barbiturates in platelets. Barbiturates, including amobarbital, butalbital, secobarbital, barbital, phenobarbital, metharbital, and primidone, were examined. Human platelet aggregation induced by adenosine diphosphate (ADP), epinephrine, and (+)-9,11-epithia-11,12-methano-thromboxane A2 (STA2), a thromboxane A2 analog, was measured using an 8-channel light-transmission aggregometer. The cytosolic free calcium concentration ([Ca2+]i) was measured by fluorometer using fura-2 loaded platelets. Inositol 1,4,5-trisphosphate (IP3) formation induced by STA2 was determined by a commercially available IP3 assay kit. Amobarbital, butalbital, and secobarbital suppressed ADP-, epinephrine- and STA2-induced platelet aggregation and the STA2-induced [Ca2+]i increase, even when Ca2+ influx was blocked by Ni2+. However, they did not affect STA2-induced IP3 formation. Barbital, phenobarbital, metharbital, and primidone (up to 1 mM) had no effect on ADP- and epinephrine-induced platelet aggregation. Thus, we conclude that amobarbital, butalbital, and secobarbital inhibit platelet aggregation by suppressing [Ca2+]i increase without affecting IP3 formation. However, these antiaggregatory effects may not have clinical importance, since the barbiturate concentrations used were higher than clinically relevant ones. The other tested barbiturates had no effects on platelet aggregation. The data indicate that the effects of barbiturates on platelet aggregation differ depending on their chemical structures.

Adult↗
PubMed1976

[Studies on the biotransformation of 5-vinyl-5-(1-methylbutyl)- and 5-vinyl-5-(1-ethyl-propyl)-barbituric acid (author's transl)].

After taking 5-vinyl-5-(1-methylbutyl)-barbituric acid (vinylbital, Speda) another not yet known metabolite (Sp 1) was isolated from urine and was identified as 5-vinyl-5-(1-methyl-3-carboxy-propyl)-bartiburic acid. Compound Sp 2a is 1-methylhydantoin. Presumably this compound is an artifact from creatinine. We have not yet been able to identify a third mercury(I)-nitrate-positive substance Sp 2b. The supposition that this compound were a metabolite of 5-vinyl-5-(1-ethyl-propyl)-barbituric acid could not be upheld. The three mercury(I)-nitrate-positive substances appearing in the urine after taking 5-vinyl-5-(1-ethyl-propyl)-barbituric acid, behaved in chromatographic analysis completely differently from the unknown compound Sp 2b. The substances were isolated. Two of them are the metabolites 5-vinyl-5-(1-ethyl-2-carboxy-ethyl)-barbituric acid and 5-(1-ethyl-propyl)-barbituric acid. We are not sure whether the third compound identified as 5-hydroxy-5-(1-ethyl-propyl)-barbituric acid, is formed in vivo, as the substance could have developed by oxidation or by the influence of peroxide contained in ether, as well. A product hydroxylized in the side chain, like in vinylbital, was not found in the metabolite urine of 5-vinyl-5-(1-ethyl-propyl)-barbituric acid.

Barbiturates↗
PubMed1975

Comparison of radioimmunoassay with thin-layer chromatographic and gas-liquid chromatographic methods of barbiturate detection in human urine.

A radioimmunoassay (I) for barbiturates was compared with thin-layer chromatographic (II) and gas-liquid chromatographic (III) methods for barbiturate detection in human urine. Timed urine samples were obtained from volunteers who had ingested 100 mg of a barbiturate. I detected barbiturate in all urines tested up to 76 h after the dose, and III in all up to 52 h and in 90% up to 76 h. II detected barbiturates in 90% of all urine samples for only 30 h, after which is reliability declined. Glutethimide interfered with radioimmunoassay of barbiturate, producing false positives. I is sensitive, reliable, and fast, and lends itself to screening large numbers of urine samples for barbiturates. For routine urine surveillance, however, we found I to be less useful than II, which is still the method of choice. I has, however, proved to be an excellent method for confirming results of II.

Adult↗
PubMed2002

Transient diffuse cerebral hypoperfusion in Tc-99m HMPAO SPECT of the brain during withdrawal syndrome following acute barbiturate poisoning.

A 29-y-old man had taken small daily doses of barbiturates as hypnotics (50 mg pentobarbital, 30 mg phenobarbital) for 4y with no evident intoxication. When he attempted suicide by ingestion of 15 g amobarbital, treatment with charcoal hemoperfusion resulted in rapid disappearance of drug from the blood. Generalized convulsions and delirium ensued; these were responsive to phenobarbital. An electroencephalogram (EEG) showed diffuse 5-Hz theta activity. Tc-99m hexamethylpropyleneamineoxime (HMPAO) single photon emission computed tomographic (SPECT) imaging of the brain demonstrated a diffuse bilateral decrease in blood flow to the cerebral cortex. These investigations were performed interictally on day4 without sedative drugs, prior to initiation of anticonvulsants, and at a time when barbiturates were no longer detected in the serum. An EEG on day 15 no longer showed abnormal slowing. On the other hand, Tc-99m HMPAO SPECT of the brain demonstrated residual cerebral hypoperfusion on day 20, with nearly full recovery of cerebral perfusion on day 51. Barbiturate withdrawal syndrome is presumed to require a history of abuse; however in patients with a history of treatment with barbiturates physicians treating acute barbiturate poisoning should be alert for the possibility of barbiturate withdrawal syndrome even in the absence of barbiturate abuse.

Adult↗
PubMedDate not supplied

[A century of barbiturates in neurology].

INTRODUCTION AND AIMS: Until the early 20th century, pharmacological treatments for neurological disorders were scarce and inefficient; only bromides stood out as sedating and antiepileptic agents. DEVELOPMENT: The introduction of barbiturates for clinical use in 1904 heralded the beginning of a new age in the pharmacological management of certain neurological pathologies. In this study, we analyse the historical process of the discovery and use of barbiturates in the field of neurology, from the moment it was started by von Baeyer in 1864, with the synthesis of malonylurea, up to the period of the decline of barbiturate therapy in the 1960s. In 1903, von Mering and Fischer discovered the hypnotic properties of barbital and later synthesised phenobarbital (1911). In the years that followed a number of barbiturates, such as butobarbital, amobarbital, secobarbital, pentobarbital, thiopental, and so on, were gradually incorporated into the therapeutic arsenal. During this period, the different therapeutic uses of barbiturates in neurology were analysed, from their traditional use as hypnotic agents (von Husen) to the discovery of the anticonvulsant properties of phenobarbital (Hauptmann) and its use in the treatment of epilepsy. CONCLUSIONS: The barbiturates were one of the first pharmacological tools that proved to be really effective in the management of some neurological disorders. Nevertheless, problems associated with their safety (dependence phenomena and deaths from overdoses), together with the introduction of numerous psychopharmacological agents in the 1950s, ended up eclipsing the use of barbiturates, except for a few very specific cases in which they are still indicated.

Anticonvulsants↗
PubMed1986

Screening for barbiturates in vitreous humor by the EMIT-st serum enzyme immunoassay.

In 16 medical examiner's cases, which were found to be barbiturate-positive by thin-layer chromatographic screening of the liver, blood barbiturate concentrations were determined by gas chromatography. The corresponding vitreous humor samples were screened by the enzyme multiplied immunoassay technique, the EMIT-st serum barbiturate assay. By using the recommended dilution for detecting serum barbiturates, it was possible to detect barbiturates in vitreous humor at a toxic concentration. By using one fourth the amount of diluent, the barbiturates could be detected also at a therapeutic concentration. The EMIT-st assay proved to be useful in the screening for barbiturates in vitreous humor, a material that is readily available in forensic toxicology.

Barbiturates↗