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PubMed1989

Effect of barbiturates on polyphosphoinositide biosynthesis and protein kinase C activity in synaptosomes.

Previously, it has been found that phenobarbital inhibited protein kinase C (PKC) and the enzymes of the metabolism of polyphosphoinositide, especially phosphatidylinositol 4-phosphate (PIP) kinase (PIP-kinase). As a continuation of these studies, a number of barbiturates (barbituric acid, barbital, butabarbital, pentobarbital, amobarbital, phenobarbital, secobarbital and hexobarbital) were tested for inhibition of these enzymes and also of phosphatidylinositol (PI) kinase (PI-kinase), in a synaptosomal preparation at pH 7.8 from the brain of rat. All compounds, except barbituric acid (and Na-barbital for PI-kinase) inhibited the three kinases. However, PKC was approximately 3-5 fold more sensitive to inhibition by the drugs (measured by Ki values) than PIP-kinase, which was 2- to 4-fold more sensitive than PI-kinase. The inhibitory potency of the drugs increased with their lipophilicity, although to a lesser degree than expected from the differences in partition coefficients; the largest deviation from a positive correlation (i.e. hexobarbital) may be the result of the blockade of an imide (-NH) group at one position of the barbituric ring. Concentrations of drugs (after correction for the greater than normal ionization (pH 7.8) of the drugs in the assays) necessary for half-maximal inhibition were well within, or smaller than, those reported necessary for in vitro blocking of nerves. The possibility, therefore, exists that the physiological effects of the barbiturates are, in part, the result of an inhibition of protein kinase C and PIP-kinase.

1-Phosphatidylinositol 4-Kinase↗
PubMed1982

Early barbiturate exposure: the brain, sexually dimorphic behavior and learning.

Barbiturates, one of the most widely prescribed and abused classes of drugs, reportedly have been prescribed in as many as 25% of pregnancies in the U.S. and Europe over the last 30 years. Nevertheless, there exists little if any data on long-term consequences of prenatal exposure to barbiturates in humans. Evidence from laboratory animals indicates that exposure to barbiturates during early developmental periods results in abnormal neural and biochemical differentiation of the central nervous system, deficits in learning, retarded attainment of developmental milestones, alteration of behavioral and physiological sex differences, increased activity, and decreased responsiveness to aversive and appetitive stimuli. Barbiturates appear to influence the brain via two routes: (1) by direct action on neural tissue; and (2) indirectly by altering hepatic metabolism of steroid hormones. It is concluded that prenatal exposure to barbiturates in human subjects may lead to learning disabilities, decreased IQ, performance deficits, increased incidence of psychosocial maladjustment, and demasculinization of gender identity and sex role behavior in males.

Animals↗
PubMed1984

The influence of barbiturate drugs on tetraethylammonium induced contractures of the chick biventer cervicis muscle in vitro.

Methohexitone sodium (METHO) 8.8 X 10(-5) M markedly potentiates tetraethylammonium (TEA)-induced contractures of the chick biventer cervicis muscle in vitro, (Elliott, 1979). A group of barbiturates were compared with METHO for their ability to potentiate TEA induced contractures. The concentrations of TEA which produced a 50% maximum contracture (EC 50) in the presence of METHO (8.8 X 10(-5) M) and in the optimum potentiating concentrations of the other barbiturates were determined. The EC 50 ratios (= EC 50 METHO/EC 50 test drug) were: barbitone sodium 0.25, phenobarbitone sodium, 0.20, pentobarbitone sodium 0.90, thiopentone sodium, 2.43. The concentrations of the barbiturates used were: barbitone 3.1 X 10(-2) M, phenobarbitone 3.15 X 10(-3) M, pentobarbitone 6.04 X 10(-4) M, thiopentone 1.89 X 10(-4) M. The EC 50 ratios were adjusted by dividing by the ratio [test barbiturate]/[METHO]. The adjusted ratios gave the following potencies (METHO = 1), barbitone 7.13 X 10(-4), n = 6, phenobarbitone 5.58 X 10(-3), n = 8, pentobarbitone 1.33 X 10(-1), n = 6, thiopentone 1.13, n = 6. The potencies correlate well with the partition coefficients of the barbiturates between cell membranes and buffer (P m/b). The regression y = 1.49x -3.12, where y = log (adjusted ratio) and x = log (P m/b) fits data with a correlation coefficient of 0.99.

Anesthetics↗
PubMed2006

Simultaneous determination of three residual barbiturates in pork using accelerated solvent extraction and gas chromatography-mass spectrometry.

A new method was developed for the rapid extraction and unequivocal determination of barbital, amobarbital and phenobarbital residues in pork. The isolation of the analytes from pork samples was accomplished by utilizing an accelerated solvent extractor ASE 300. The procedure was automatically carried out in series for fat removing and extraction, respectively with n-hexane and acetonitrile pressurized constantly at 10.3 MPa for 30 min. After evaporation, the extracts were cleaned up on a C(18) solid phase extraction (SPE) cartridge and the barbiturates were eluted with hexane-ethyl acetate (7:3), evaporated on a rotary evaporator and derivatized with CH(3)I. The methylated barbiturates were separated on a HP-5MS capillary column and detected with a mass detector. Electron impact ion source (EI) operating in time program-selected ion monitoring mode (SIM) was used for identification and external standard method was used for quantification. Good linearity was obtained in the range from 0.5 microg/kg to 25 microg/kg. Average recoveries of the three barbiturates spiked in pork ranged from 84.0% to 103.0%, with relative standard deviations from 1.6% to 12%. The limit of detection (LOD) was 0.5 microg/kg for the three barbiturates (S/N>or=3). The quantification limit (LOQ) was 1 microg/kg for the three barbiturates (S/N>or=10).

Animals↗
PubMed2003

Barbiturates for acute neurological and neurosurgical emergencies--do they still have a role?

A number of clinical studies have reported poor clinical outcomes for patients treated with barbiturate therapy in acute neurological and neurosurgical emergencies. Barbiturate therapy, as currently practised with thiopentone and pentobarbitone at least, is also associated with a prolonged post-infusion period of clinical unresponsiveness. Hence, the popularity of barbiturate therapy for sedation of critically ill neurological and neurosurgical patients has declined over the past decade. A retrospective study of traumatic brain injury patients treated at the Royal North Shore Hospital, Sydney, with high-dose thiopentone therapy between 1987 and 1997 has found disappointing results with a 1-month mortality outcome of 50% (14 of 28 patients). Nevertheless, barbiturate therapy remains a consideration for patients with severe cranial trauma in whom preferred treatments have failed to control intracranial or cerebral perfusion pressures. More favourable results ( approximately 10% 1-month mortality rate) were encountered for patients with refractory vasospasm complicating subarachnoid haemorrhage or intracerebral haemorrhage complicating supratentorial arteriovenous malformation resection. A well designed, prospective and randomised controlled trial may be of value in further determining the role of barbiturate therapy in acute neurovascular emergencies refractory to standard therapy.

Barbiturates↗
PubMed1983

Structure-activity relationships of convulsant and anticonvulsant barbiturates: a computer-graphic-based pattern-recognition analysis.

A computer-graphic-based pattern-recognition study of two series of 5-ethyl-5-substituted barbiturates has been undertaken in an attempt to find a correlation between molecular conformation and convulsant and anticonvulsant activity. Studies of a first (trial) set of barbiturates related to pentobarbital revealed a region of space in which at least one low-energy conformation of the hydrocarbon side chain of each of the anticonvulsant barbiturates resides. Another region was occupied by a low-energy conformation of each of the convulsant barbiturates. These regions of space are, thus, possible pharmacophores for convulsant and anticonvulsant activity. Analysis of a second (test) set of barbiturates related to phenobarbital has shown that the activities and structures of these molecules are consistent with the above model. These pharmacophores thus provide a basis for the design of rigid, new analogues with potent convulsant or anticonvulsant activities.

Anticonvulsants↗
PubMed1981

Barbiturate and hypnosedative withdrawal by a multiple oral phenobarbital loading dose technique.

Although intravenous phenobarbital loading is effective in barbiturate withdrawal, controlled infusions of a drug are inconvenient. To develop a practical and more widely applicable method, oral loading doses of phenobarbital were given to 21 barbiturate addicts, whose estimated mean daily intake of barbiturates was 1 gm (range 0.5 to 4 gm). Twelve had a past or present history of barbiturate withdrawal seizures. Phenobarbital was given orally at a rate of 120 mg/hr until a predetermined clinical end point of phenobarbital effect was achieved. This end point was the presence of at least three of the following: nystagmus, drowsiness, ataxia, dysarthria, or emotional lability. The total phenobarbital loading dose (mean +/- SD) was 23.4 +/- 7.1 mg/kg, median phenobarbital concentration after loading was 35.9 mg/l (range 13.2 to 71.6 mg/l), and median half-life (t 1/2) of phenobarbital was 90 hr (range 38 to 240 hr). One patient with t 1/2 = 38 hr was given supplemental doses of phenobarbital. None developed seizures or other evidence of barbiturate withdrawal.

Administration, Oral↗
PubMed1994

Enhancement of hepatocarcinogenesis and induction of specific cytochrome P450-dependent monooxygenase activities by the barbiturates allobarbital, aprobarbital, pentobarbital, secobarbital and 5-phenyl- and 5-ethylbarbituric acids.

To test predictions that barbiturates which are long-acting sedatives and/or strong inducers of CYP2B-mediated monooxygenase activities would be effective promoters of hepatocarcinogenesis, a series of clinically-useful barbiturates and structural analogs were tested for ability to promote hepatocellular carcinogenesis in male F344/NCr rats initiated with N-nitrosodiethylamine and for efficacy as inducers of CYP2B activity in non-initiated rats of the same sex and strain. The barbiturates were administered in the diet at concentrations equimolar to 500 p.p.m. of the known liver tumor promoter phenobarbital, which served as the positive control for this study. Phenobarbital, which has the longest duration of sedative action of this series of compounds, caused the greatest induction of CYP2B activity, and displayed strong liver tumor promoting effects. Allobarbital and aprobarbital, two intermediate-duration sedatives, were found to promote hepatocarcinogenesis, with allobarbital proving to be as effective as phenobarbital in this respect and aprobarbital being somewhat weaker as a promoter. These intermediate-duration sedatives were each relatively weak CYP2B-type inducers, causing approximately 25% of the induction displayed by phenobarbital. The nonsedatives, 5-phenyl- and 5-ethyl-barbituric acids, were essentially inactive as CYP2B-type inducers and were also found to be relatively inactive as promoters of hepatocarcinogenesis. Of the shorter-duration sedatives, pentobarbital was found to promote, and was relatively effective as a CYP2B-type inducer, while secobarbital showed little or no promoting activity and was less effective as an inducer of CYP2B activities. Pentobarbital thus proved an important exception to our hypothesis that only long-acting sedative barbiturates would promote hepatocarcinogenesis. Although both the durations of sedative action and the degrees of CYP2B-type induction exhibited by these compounds correlate with a quantitative parameter for liver tumor-promoting activity (relative promotion index), neither parameter appears to be sufficient, by itself, as a predictor of promoting activity for rat liver.

Animals↗
PubMed1982

Comparison of enhancement of GGTase-positive foci and induction of ornithine decarboxylase in rat liver by barbiturates.

The indication of ornithine decarboxylase (ODC) by barbiturates and the ability of barbiturates to enhance neoplastic progression of chemically initiated cancer was examined in rat liver. All seven barbiturates induced ODC with barbital (7.7 fold increase) and phenobarbital (5.7 fold increase) demonstrating the most potent activity. Maximum induction of ODC by phenobarbital was obtained in 18 h. Barbital (500-5000 p.p.m.) and phenobarbital (500 p.p.m.) administered in the drinking water enhanced the appearance of diethylnitrosamine (DENA)-initiated gamma- glutamyltranspeptidase (GGTase)-positive foci. Amobarbital, hexabarbital and pentabarbital did not enhance the appearance of GGTase-positive foci. In the absence of previous initiation by DENA, the enhancing regimen of the barbiturates did not cause the appearance of GGTase-positive foci. Barbiturates induced ODC activity in rat liver and enhanced the incidence of DENA initiated GGTase-positive foci.

Animals↗
PubMed1987

Induction of alkoxyresorufin O-dealkylases, epoxide hydrolase, and liver weight gain: correlation with liver tumor-promoting potential in a series of barbiturates.

The effects of a series of barbiturates, of known and varying liver tumor-promoting ability, on several short-term endpoints including liver weight and liver-to-body weight ratio increases and induction of cytochromes(s) P-450 and epoxide hydrolase activities were examined. Male F344 rats (3 months of age) were administered barbiturates in the drinking water for 12 days. At the end of the treatment period they were killed, body and liver weights were taken, microsomal p-nitroanisole O-demethylation and epoxide hydration, and liver S-9 O-dealkylation of ethoxy-, pentoxy- and benzyloxyresorufin were measured. The latter two substrates have been shown to be preferentially metabolized by the major phenobarbital-inducible form of cytochrome(s) P-450 (P-450b), and were employed since they offered a means of differentiating more clearly varying levels of P-450 induction. Exposure to sodium barbital (SB) and sodium phenobarbital (PB) resulted in significant increases in liver weight and liver-to-body weight ratios. Induction of cytochrome(s) P-450 and epoxide hydrolase activities by the various barbiturates depended on the functional groups on C5. When ranked in terms of decreasing induction potency, the following order was obtained for each enzyme activity quantitated: PB, SB, sodium pentobarbital, amobarbital, hexobarbital and the C5-unsubstituted parent compound (barbituric acid). Thus, the barbiturates were found to exhibit a spectrum of induction potencies, with PB and SB, the most potent liver tumor promoters, yielding the greatest degree of liver weight increase and induction of cytochrome(s) P-450 and epoxide hydrolase activities.

7-Alkoxycoumarin O-Dealkylase↗
PubMed2001

Use of a statistically designed experimental approach to optimize the propylketal derivatization of barbiturates.

The derivatization of barbiturates with dimethylformamide dipropylacetal and dimethylformamide diisopropylacetal is studied with respect to the optimization of reaction recovery and reliability. A second-order orthogonal experimental design is utilized in order to obtain regression equations for the reaction recovery dependence on the derivatization solution composition, incubation temperature, and time for amobarbital, butalbital, pentobarbital, phenobarbital, and secobarbital. Regression equations for the effect of incubation temperature and time on the derivative recovery and the optimum conditions for derivatization recoveries are obtained. Differences in the phenomena of the derivative formation are evaluated between the two derivatizing reagents and the barbiturates. Based on the analysis of the obtained equations, it is concluded that the dipropylketal derivative of barbiturates is superior in comparison with diisopropylketal when considering the milder conditions of the reaction, absence of sudden changes in the recovery with a variation in the derivatization parameters, and reliability for the simultaneous testing of the barbiturates. A method for the routine testing of the barbiturates by gas chromatography-mass spectrometry in urine specimens is included.

Barbiturates↗
PubMed1999

Barbiturates and lung cancer: a re-evaluation.

BACKGROUND: Barbiturates, particularly phenobarbital, have been shown to be a tumour promoter in animal experiments and were found to be associated with increased risk of lung cancer in our cohort follow-up study to screen pharmaceuticals for possible carcinogenic effects. Sixteen more years of follow-up have accumulated permitting a more detailed evaluation of this association. METHODS: In all, 10,213 subscribers of the Kaiser Permanente Medical Care Program who received barbiturates between 1969 and 1973 from its San Francisco pharmacy were followed up through 1992 and their incidence of lung cancer at biennial intervals was compared with what was expected based on the experience of the entire pharmacy cohort (143,594). Smoking-habit data were available on about half of the barbiturate users and were used to adjust for cigarette smoking in both the observed/expected analysis and in Cox proportional hazards analysis. RESULTS: The initially elevated standard morbidity ratio of 1.55 (95% CI: 1.25-1.91) with 3-7 years of follow-up gradually decreased and stabilized at about 1.3 after 11-15 years of follow-up. This trend for diminishing relative risk over time was more pronounced among the never smokers but their initial excess risk was not statistically significant due to small numbers. A dose-response trend was observed, based on the number of prescriptions dispensed. Analytical control for cigarette smoking reduced but did not eliminate either the association or the dose-response trend. Most of the barbiturate-associated cases in never smokers were women and the predominant histological type was adenocarcinoma. CONCLUSIONS: These findings from up to 23 years of follow-up are not conclusive because of the continuing small number of never smokers who developed lung cancer. However, they strengthen and refine previous observations of a barbiturate-lung cancer association, which is probably not fully explained by confounding by cigarette smoking. The diminution of excess risk over time is consistent with a tumour promoter effect. Findings among the never smokers suggest that this possible effect may be greatest on adenocarcinomas in women.

Adenocarcinoma↗
PubMed1986

Drug use and interpersonal violence. Barbiturates detected in homicide victims.

To characterize patterns of barbiturate use in homicide victims, we used data from the Los Angeles City Police Department and the Medical Examiner-Coroner's Office to study 4,950 victims of criminal homicide committed in that city in 1970-1979. Barbiturates were detected in 323 (7.9 per cent) of the 4,063 victims who were tested. Detectable levels were present most often in black victims (10.4 per cent), in equal proportions of Anglos and Hispanics (6 per cent), and least often among victims in other race-ethnic groups (4.1 per cent). Among specific subgroups, barbiturate use was greatest in black female victims (15.1 per cent). The detection of barbiturates more commonly among certain subgroups and in specific types of homicidal encounters suggests that barbiturate use may be linked to specific behaviors that precede homicide.

Barbiturates↗
PubMed1999

Preparation of barbiturate optical isomers and their effects on GABA(A) receptors.

BACKGROUND: Barbiturate anesthetics are optically active and usually exist in two mirror-image enantiomeric forms. Their stereoselective effects in mammals are well known, but remarkably few data are available concerning their effects on anesthetic targets in vitro. This is in part because of the lack of availability of pure barbiturate enantiomers. Such in vitro data could be used to test the relevance of putative molecular targets. METHODS: A high-performance liquid chromatography technique using a permethylated beta-cyclodextrin column was used to separate the optical isomers of three barbiturates in preparative quantities. The effects of the isomers on GABA-induced currents in stably transfected mouse fibroblast cells were investigated using the whole-cell patch-clamp technique. RESULTS: Highly purified optical isomers of hexobarbital, pentobarbital, and thiopental were prepared, and their effects were studied on a gamma-aminobutyric acid type A receptor of defined subunit composition. For each of the three barbiturates, both enantiomers potentiated gamma-aminobutyric acid-induced currents at pharmacologically relevant concentrations, with the S-enantiomer being more potent than the R-enantiomer by a factor of between 1.7 and 3.5. The degree of stereoselectivity did not vary greatly with anesthetic concentration. CONCLUSIONS: The rank order and degree of stereoselectivity that we have observed for the enantiomers of hexobarbital, pentobarbital, and thiopental acting on the gamma-aminobutyric acid type A receptor are entirely consistent with this receptor playing a central role in the anesthetic actions of barbiturates.

Animals↗
PubMed2000

Effect of barbiturates on hydroxyl radicals, lipid peroxidation, and hypoxic cell death in human NT2-N neurons.

BACKGROUND: Barbiturates have been shown to be neuroprotective in several animal models, but the underlying mechanisms are unknown. In this study, the authors investigated the effect of barbiturates on free radical scavenging and attempted to correlate this with their neuroprotective effects in a model of hypoxic cell death in human NT2-N neurons. METHODS: Hydroxyl radicals were generated by ascorbic acid and iron and were measured by conversion of salicylate to 2,3-dihydroxybenzoic acid. The effect of barbiturates on lipid peroxidation measured as malondialdehyde and 4-hydroxynon-2-enal was also investigated. Hypoxia studies were then performed on human NT2-N neurons. The cells were exposed to 10 h of hypoxia or combined oxygen and glucose deprivation for 3 or 5 h in the presence of thiopental (50-600 microM), methohexital (50-400 microM), phenobarbital (10-400 microM), or pentobarbital (10-400 microM), and cell death was evaluated after 24 h by lactate dehydrogenase release. RESULTS: Pentobarbital, phenobarbital, methohexital, and thiopental dose-dependently inhibited formation of 2,3-dihydroxybenzoic acid and iron-stimulated lipid peroxidation. There were significant but moderate differences in antioxidant action between the barbiturates. While phenobarbital (10-400 microM) and pentobarbital (10-50 microM) increased lactate dehydrogenase release after combined oxygen and glucose deprivation, thiopental and methohexital protected the neurons at all tested concentrations. At a higher concentration (400 microM), pentobarbital also significantly protected the neurons. At both 50 and 400 microM, thiopental and methohexital protected the NT2-N neurons significantly better than phenobarbital and pentobarbital. CONCLUSIONS: Barbiturates differ markedly in their neuroprotective effects against combined oxygen and glucose deprivation in human NT2-N neurons. The variation in neuroprotective effects could only partly be explained by differences in antioxidant action.

Barbiturates↗
PubMed1978

Thyrotrophin, prolactin and growth hormone responses to TRH in barbiturate coma and in depression.

The effects of 200 microgram thyrotrophin-releasing hormone (TRH) i.v. on thyrotrophin (TSH), prolactin (PRL), growth hormone (GH) and triiodothyronine (T3) were studied in eight patients with barbiturate coma due to attempted suicide, in the same patients after recovery, in eight depressive patients and in eight normal controls. The patients with barbiturate coma presented normal basal TSH and PRL, elevated basal GH and normal PRL but blunted TSH responses to TRH; their GH concentrations varied widely without consistent relation to TRH administration. The same patients after recovery from coma presented normal TSH and PRL, slightly elevated basal GH, and normal PRL but blunted TSH responses to TRH; in four of these patients, a clear-cut rise in GH (i.e. more than 10 ng/ml) occurred after TRH administration. The depressive patients presented normal basal TSH and PRL, slightly elevated basal GH, and normal PRL but blunted TSH responses to TRH; in four of these patients, a moderated rise in GH (less than 10 ng/ml) occurred after TRH administration. The increment in T3 concentrations 120 min after TRH was found reduced in the comatose patients only. Basal cortisol was measured in all the subjects and found elevated in the comatose patients only. It is concluded that the abnormal TSH and GH responses to TRH observed in patients with barbiturate coma are more likely related to depressive illness than to an effect of barbiturates at the pituitary level. Barbiturates might affect thyroid secretion.

Adolescent↗
PubMed1986

A trial of discontinuation of barbiturates in patients with secondary generalized epilepsy.

The vast majority of patients with secondary generalized epilepsy (SGE) were under polytherapy including barbiturates. We were able to completely withdraw barbiturates in 17 cases with a refractory course of SGE. Valproic acid (VPA) is considered as one of the best drugs for SGE. Barbiturates decrease the serum level of VPA and this may lead to a reduced efficacy of VPA. The dosage of VPA was adjusted to attain the level of 100-150 micrograms/ml. Barbiturates were then gradually decreased and finally discontinued. After six months of follow-up, 13 patients (76%) showed a reduced seizure frequency. Also, the physical and psychological conditions improved in a good number of cases. Barbiturates are not necessarily required in pharmacotherapy of SGE and may be safely withdrawn.

Adolescent↗
PubMed1991

Barbiturates inhibit ATP-K+ channels and voltage-activated currents in CRI-G1 insulin-secreting cells.

1. Patch-clamp recording techniques were used to examine the effects of barbiturates upon the ATP-K+ channel, and voltage-activated channels present in the plasma membrane of CRI-G1 insulin-secreting cells. 2. Thiopentone inhibited ATP-K+ channel activity when applied to cell-attached patches or the intracellular or extracellular surface of cell-free patches. Secobarbitone and pentobarbitone were also effective inhibitors of ATP-K+ channels in cell-free patches, whereas phenobarbitone was ineffective. 3. The diabetogenic agent, alloxan, which is structurally related to the barbiturates also produced an inhibition of ATP-K+ channel activity in outside-out patches. 4. Whole-cell ATP-K+ currents were used to quantify the effects of the barbiturates: concentration-inhibition curves for thiopentone, secobarbitone and pentobarbitone resulted in IC50 values of 62, 250 and 360 microM respectively. Phenobarbitone at a concentration of 1 mM was virtually ineffective. 5. Calculation of the apparent membrane concentrations for these drugs indicate that for a given degree of ATP-K+ channel inhibition a similar concentration of each barbiturate is present in the membrane. This suggests that hydrophobicity plays a primary role in their mechanism of action. The pH-dependence and additive nature of barbiturate block also indicates a membrane site of action. 6. Thiopentone, (100 microM) was also found to inhibit differentially voltage-activated whole-cell currents. The relative potency of thiopentone at this concentration was 0.64, 0.38 and 0.12 for inhibiting Ca2+, K+ and Na+ currents respectively when compared with its ability to inhibit the ATP-K+ channel.

Adenosine Triphosphate↗