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PubMedDate not supplied

GLC screening and confirmation of barbiturates in post mortem blood specimens.

A quantitative gas chromatographic (GC) method for the screening and confirmation of barbiturates in post mortem blood specimens is presented. Barbiturates were extracted from blood samples and the extracts cleaned-up, concentrated, and then analyzed as free drugs on a 10% UCW-982 GC column. Samples screened positive for free barbiturates were methylated to form 1,3-dimethylbarbiturates, which were then chromatographed on a 3% SE-30 column to confirm the barbiturate identity.

Barbiturates↗
PubMed1975

Barbiturates and aortic and venous smooth-muscle function.

Using isolated rat aortic strips (AS) and portal veins (PV), it was found that all of the barbiturates studied (thiopental, secobarbital, pentobarbital, amobarbital, phenobarbital, and barbital): a) inhibit development of spontaneous mechanical activity (vasomotion) in AS and PV in concentrations used to induce surgical anesthesia or concentrations used for anticonvulsive therapy; b) dose-dependent attenuate contractions induced by epinephrine and potassium (K+); c) cause non-competitive displacement of the dose-response curves of these vasoactive compounds; d) attenuate calcium (Ca++)-induced contractions of K+-depolarized AS and PV; e) rapidly relax drug-induced, as well as Ca++-induced, contractions of AS and PV. In addition, the data indicate that: a) rat portal venous smooth muscle is more sensitive to the inhibitory actions of barbiturates than is rat aortic smooth muscle, and b) thiopental, but none of the other barbiturates, can elicit dose-dependent contractions of AS. Concentrations of barbiturates known to be present during induction of surgical anesthesia can exert depressant effects on at least two types of vascular smooth muscle that may be related to actions on movement and/or translocation of Ca++.

Amobarbital↗
PubMed1981

Abnormal temperature control after intoxication with short-acting barbiturates.

Changes in rectal and toe temperatures were measured in 16 patients who had been intoxicated with short-acting barbiturates. The lowest temperatures observed in the group of 16 patients averaged 35.5 +/- 2.0 degrees C. In 11 patients, the interval between intoxication and admission was documented. There was a significant correlation (r = 0.83) between the time of estimated intoxication and hypothermia. Patients who were admitted soon after the ingestion of the barbiturates had the lowest rectal temperatures. These observations indicate that hypothermia is a usual clinical sign in the initial period after intoxication with a short-acting barbiturate. Except for 2 patients, rectal temperature exceeded 38 degrees C during the interval of recovery with the maximum rectal temperature averaging 39.0 +/- 0.8 degrees C. Hyperthermia was not related to infection of the airways, lungs, urinary tract, or bloodstream. In 11 patients, pathogenic organisms were recovered from the airway and/or urine, but there was no difference in the highest rectal temperature in these patients (39.0 +/- 0.9 degrees C) when compared with 5 patients from whom no pathogenic organisms were recovered (39.2 +/- 0.7 degrees C). Accordingly, there was no evidence that hyperthermia was due to infection. The skin temperatures of the ventrum of the first toe were not typically decreased during hypothermia. To the contrary, increases in skin temperatures were often observed during hypothermia. These observations provide evidence of altered thermoregulation with increased surface heat loss accounting for the hypothermia in the early course and heat conservation with hyperthermia during the later course of intoxication by short-acting barbiturates.

Adolescent↗
PubMed1980

Barbiturate therapy in cerebral ischaemia.

Experimental and clinical studies of the protective effect of barbiturates in cerebral ischaemia are reviewed. Their action in protecting the brain from the effects of ischaemia is related to their action as anaesthetic agents and probably to the depression of neuronal function and metabolism but is incompletely understood. Their effect is dose related. Early administration is likely to be crucial to the success of barbiturate therapy as secondary events following an episode of cerebral ischaemia can lead to irreversible brain damage within 2--3 h. A potential collateral circulation appears to be essential for the protective effect of barbiturates. There may be a possibility of partly overcoming time delays in administration by giving larger doses of barbiturates.

Animals↗
PubMed1973

Barbiturate-induced transmitter release at a frog neuromuscular junction.

1. The influence of barbiturates on neuromuscular transmission at end-plates of frog sartorius muscles was investigated electrophysiologically on preparations bathed in Ringer solution containing a low concentration of calcium and a high concentration of magnesium.2. Effects of a convulsant barbiturate, 5-(2-cyclohexylideneëthyl)-5-ethyl barbituric acid (CHEB), were compared with those of phenobarbitone.3. CHEB and phenobarbitone increased the mean quantum content of the end-plate potentials and decreased the mean amplitude of the miniature end-plate potentials.4. Both barbiturates enhanced the duration of the nerve-terminal action potential and had little or no effect on the effective resistance of the skeletal muscle membrane.

Action Potentials↗
PubMed1973

Mechanisms contributing to barbiturate intolerance in rats.

1. Female rats, 3 weeks after pretreatment with 200 or 400 (mg/kg)/day barbitone for 2 or 30 days, exhibited a prolonged sleeping time and a reduced awakening barbiturate brain level when challenged with either barbitone or pentobarbitone. After 3 additional weeks, the latter responses had returned, or were returning to, control values.2. Barbitone pretreatment schedules had no residual effect upon in vitro hepatic pentobarbitone-metabolizing activity measured 3 or 6 weeks later, except in one instance, when hepatic enzyme activity was significantly enhanced 3 weeks after 30 daily doses of 200 mg/kg barbitone. In this case, however, an enhanced barbiturate sleeping time, together with a reduced awakening barbiturate brain level, were observed.3. It is concluded that barbitone administered intraperitoneally in doses of 200 to 400 (mg/kg)/day for 2 or 30 days induces a non-hepatogenic intolerance to barbiturates, related to an increased sensitivity of the central nervous system to these drugs. This central intolerance is seen 3 weeks, but not 6 weeks, after pretreatment. Furthermore, this central intolerance has been observed to co-exist with an hepatic tolerance, a situation which could result in a reduced LD(50) coupled with an increase in ED(50).

Animals↗
PubMed1983

Barbiturates increase the rate of voltage-dependent inactivation of the calcium current in snail neurones.

Effects of barbiturates (thiopentone, pentobarbitone, phenobarbitone and barbitone) on the calcium current (ICa) in identified Helix neurones were studied, using a conventional suction pipette technique. Barbiturates depressed the maximal peak amplitudes (MPA) of ICa in a dose-dependent manner without shifting the current-voltage relationships along the voltage axis. Barbiturates accelerated the decay phase of ICa at high concentrations (1 X 10(-4) to 3 X 10(-3) M), at which concentrations double-pulse experiments showed the increased rate of a voltage-dependent inactivation of ICa. It is concluded that the acceleration of the decay phase of ICa by barbiturates may be due to the increased rate of the voltage-dependent inactivation of ICa.

Animals↗
PubMed1975

Mechanism of induction of hepatic microsomal drug metabolizing enzymes by a series of barbiturates.

The inducing effect of certain barbiturates (secobarbitone, thiopentone, pentobarbitone, allobarbitone, phenobarbitone and barbitone) on the levels of the hepatic microsomal drug-metabolizing enzymes has been studied in the rat both in vivo and in vitro. The extent of induction was related to the plasma half-lives of the barbiturates; compounds with low rates of metabolism and long half-lives were the most potent inducing agents. The latter (phenobarbitone, pentobarbitone and allobarbitone) were shown by spectral technique to interact with cytochrome P-450 suggesting that their mechanism of enzyme induction was 'substrate induction' in type. Barbiturates containing an allyl group (secobarbitone and allobarbitone) had a weaker inducing effect than expected, possibly due to their destruction of cytochrome P-450. Despite its short plasma half-life of 0-5 h thiopentone was a relatively potent inducer probably due to its metabolism to pentobarbitone, which has a much longer plasma half-life (1-3 h). Barbitone is an effective inducer of the drug-metabolizing enzymes, yet does not interact spectrally with cytochrome P-450; this is in accord with the observations that although there are increases in NADPH-cytochrome c reductase and cytochrome b5, following administration of barbitone there is no increase in cytochrome P-450. Barbiturate pretreatment does not affect the activities of glucose-6-phosphatase, glucose-6-phosphate dehydrogenase or 6-phosphogluconate dehydrogenase.

Animals↗
PubMed1972

Destruction of cytochrome P 450 by secobarbital and other barbiturates containing allyl groups.

Administration of certain commonly used barbiturates containing allyl groups, such as secobarbital, allobarbital, or aprobarbital to rats treated chronically with a microsomal enzyme inducer causes a rapid destruction of the liver microsomal hemoprotein that serves as the terminal oxidase for drug metabolism. In contrast, barbiturates without an allyl group do not have this effect. The decrease in this hemoprotein, cytochrome P(450), by the barbiturates containing an allyl group could also be demonstrated in an in vitro liver microsomal system requiring reduced nicotinamide adenine dinucleotide phosphate. These results suggest that the barbiturates containing an allyl group are converted to a metabolite that leads to the destruction of cytochrome P(450).

Alkenes↗
PubMed1982

Barbiturates depress vagal motor pathway to ferret trachea at ganglia.

To determine which site in the vagal motor pathway to airway smooth muscle is most sensitive to depression by barbiturates, we recorded isometric muscle tension in vitro and stimulated the vagal motor pathway at four different sites before and after exposure to barbiturates. In isolated tracheal rings from ferrets, we stimulated muscarinic receptors in the neuromuscular junction by exogenous acetylcholine, postganglionic nerve fibers by electrical fluid stimulation, and the postsynaptic membrane in ganglia by 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP). We also developed a tracheal nerve-muscle preparation to stimulate preganglionic fibers in the vagus nerve electrically. Activation of ganglia by DMPP or by vagus nerve stimulation was depressed by barbiturates at 10-fold lower concentrations than those depressing the activation of postganglionic nerves or the neuromuscular junction. These findings suggest that the postsynaptic membrane in parasympathetic ganglia is the site in the vagal motor pathway most sensitive to depression by barbiturates.

Animals↗
PubMed1977

Barbiturate-induced choleresis: possible independence from microsomal enzyme induction.

The influence of four barbiturates, phenobarbital, barbital, thiopental, and pentobarbital, on bile secretion and on the hepatic microsomal system was studied in anesthetized rats. The barbiturates were injected intraperitoneally for 4 days and the animals were studied on the 5th day. It was found that: (1) phenobarbital, barbital, and thiopental, but not pentobarbital, significantly increased liver weight, cytochrome P-450 concentration in the liver, decreased pentobarbital sleeping time and induced a hypertrophy of the smooth endoplasmic reticulum in the hepatocytes at electron microscopy; (2) in contrast, the four barbiturates, including pentobarbital, significantly increased bile flow; this increase was attributed to an increase in the bile acid independent bile flow. There was no correlation between the increase in bile flow and the cytochrome P-450 concentration in the liver. It is concluded that the increase in bile flow observed after barbiturate treatment in the rat is possibly independent of the hepatic microsomal enzyme induction produced by these drugs.

Animals↗
PubMed1983

Quantification of the interaction between barbiturates and alcohol and interpretation of fatal blood concentrations.

Barbiturates and alcohol are frequently found in combination in cases of accidental or intentional fatal self-poisoning. Unfortunately, the lack of any precise knowledge concerning their interaction creates difficult problems when an interpretation of toxicological data is sought. 1 In the following work the joint action of single barbiturates and alcohol is examined and a means of quantifying it is presented. 2 The effects of different amounts of alcohol on fatal amylobarbitone, butobarbitone, pentobarbitone, phenobarbitone and quinalbarbitone blood concentrations are compared. 3 Combined alcohol-barbiturate blood concentration curves connecting those concentration pairs equally effective in causing death are used to quantify the increase in toxicity. The quantitative effects of alcohol appear to be greater with the shorter- and longer-acting barbiturates than with the intermediate-acting derivatives. The different modes of interaction are discussed in terms of the physico-chemical and pharmacokinetic properties of the drugs.

Barbiturates↗
PubMed1991

The effects of the falling therapeutic and subtherapeutic barbiturate blood levels on electrocerebral silence in clinically brain-dead children.

In a retrospective study at a large children's hospital, we identified 92 children who had received barbiturates that were simultaneously discontinued at the time they were being evaluated for brain death in the presence of electrocerebral silence and clinical brain death by physical exam. Of these 92 children, 67 had barbiturate levels that were monitored from initial therapeutic or subtherapeutic levels. Repeat EEGs were obtained in 76 patients, and in all electrocerebral silence and clinical brain death (by exam) persisted despite the lower barbiturate levels. The study suggests that therapeutic and subtherapeutic barbiturate levels have no effect on the outcome of children who fulfill the criteria for brain death.

Adolescent↗
PubMed2006

Kinetic study on the photostability of riboflavin in the presence of barbituric acid.

The photochemical fate of riboflavin (vitamin B2) in the presence of barbituric acid was examined employing polarographic detection of dissolved oxygen and steady-state and time-resolved spectroscopy. Under visible light, riboflavin reacts with barbituric acid--the latter being transparent to this type of photo-irradiation--via radicals and reactive oxygen species, such as singlet molecular oxygen [O2(1delta(g))] and superoxide radical anion, which are generated from the excited triplet state of the vitamin. As a result, both the vitamin and barbituric acid are photodegraded. Kinetic and mechanistic studies on the photoreactions of riboflavin in the presence of barbituric acid indicate the excellent quenching ability of the latter towards O2(1delta(g)).

Barbiturates↗
PubMed1980

Treatment of ischemic deficits from cerebral vasospasm with high dose barbiturate therapy.

In 12 patients with life-threatening neurological deficits from vasospasm refractory to other measures, high dose barbiturate therapy was used in an attempt to prevent permanent changes in the brain. In each case angiography was performed and intracranial pressure was measured. Dexamethasone, a low molecular weight dextran, and mannitol were administered. If intracranial pressure (ICP) was elevated, drainage of cerebrospinal fluid and hyperventilation were used. Arterial pressure was maintained at not less than 140/90 preoperatively and 180/100 postoperatively. Barbiturate therapy was continued until vasospasm decreased angiographically and ICP was normal. Eleven of the 12 patients perished. One had a fatal rebleed. One died of an iatrogenic hemothorax. Four died from uncontrollable intracranial hypertension. One improved slightly and then died from a cardiac arrhythmia. One died of increased ICP when her ventriculostomy malfunctioned. One improved and was responding purposefully to pain, only to die suddenly with a low ICP. Two patients became awake and responsive to verbal commands; 1 of these died from Klebsiella meningitis and the other died from an intracerebral hematoma. In the 3 patients in whom hypothermia was also used, profound alterations in acid-base and fluid electrolyte balance occurred. These discouraging results are most likely a reflection of the severity of the patients' condition at the beginning of therapy. There may be some benefit of barbiturates in the management of vasospasm, and the potential effectiveness of barbiturates may be more obvious if therapy is started at an earlier stage. However, until further evidence of the usefulness of this modality becomes manifest, it should be limited to patients with life-threatening impairments unresponsive to all other measures.

Adolescent↗
PubMed1983

Effect of acetazolamide on barbiturate-induced sleeping time in mice. III. Pharmacokinetics of serum elimination and brain distribution.

Effects of acetazolamide (AZA) on the serum elimination and brain distribution of barbital (BA), phenobarbital (PHB), pentobarbital (PEB) and hexobarbital (HB) were studied in mice. When the barbiturates were administered intraperitoneally to mice, the pretreatment of AZA reduced the serum BA and PHB levels, and significantly increased these brain levels. While relatively small and no effects of AZA were observed for the PEB and HB levels, respectively. After the intravenous administration, the serum elimination of these barbiturates were described by the two compartment model. Although the pretreatment of AZA tended to increase the volumes of central compartment and decrease the elimination rate constants for BA, PHB and PEB, the elevated brain levels of the barbiturates could not be explained as the simulated peripheral concentrations. However, it appeared that the prolongation effect of AZA on the BA, PHB and PEB sleeps in mice was associated with the elevated brain barbiturate levels with AZA.

Acetazolamide↗
PubMed2000

Evaluation of Emit tox benzodiazepine and barbiturate assays on the Vitalab Viva analyser and FPIA on the Abbott ADx analyser.

We evaluated the performance of the Emit tox benzodiazepine and barbiturate assays (Dade Behring) and fluorescence polarisation immunoassay (FPIA) (Abbott) for use with serum determinations in preliminary therapeutic drug monitoring or acute drug intoxication detection. Performance, as indicated by CVs, of the Emit tox benzodiazepine and barbiturate assays and FPIA showed that both immunochemical techniques are precise and have good reproducibility. For within-run studies, results from benzodiazepine determinations showed maximum CV values of 1.91% for the Emit method and 2.65% for FPIA; results from barbiturate determinations showed maximum CV values of 2.01% for the Emit method and 1.89% for FPIA. For between-run studies, results from benzodiazepine determinations showed maximum CV values of 1.79% for the Emit method and 1.12% for FPIA; results from barbiturate determinations showed maximum CV values of 2.09% for the Emit method and 2.02% for FPIA.

Barbiturates↗
PubMed1994

Relationship of cerebral blood flow, cerebral metabolism, and electroencephalography to outcome in acute experimental compression ischemia--barbiturate effects on delayed brain swelling.

Acute compression ischemia was induced in 30 cats by progressive inflation of an epidural balloon, followed by rapid decompression. Changes in intracranial pressure, mean arterial blood pressure, cerebral blood flow (CBF), arteriovenous oxygen difference (AVDO2), cerebral metabolic rate of oxygen (CMRO2), and electroencephalography (EEG) were studied in 13 untreated animals and in seven animals receiving barbiturate. Ten cats with cardiovascular or respiratory problems, or intracranial hematoma were excluded from the study. In untreated animals, six (46%) survived with no brain swelling and were classified as the "no swelling group," and seven (56%) died from fatal brain swelling and were classified as the "delayed swelling group." All animals with barbiturate therapy showed no brain swelling. Serial measurement of CBF, AVDO2, and CMRO2 indicated the existence of postischemic delayed hypoperfusion associated with relative hypermetabolism in untreated animals. Good recovery of CBF and CMRO2 was observed in the "no swelling group," and poor recovery in the "delayed swelling group." The time course of the total fast-wave components on EEG was quite similar to that of CMRO2, and the time course of the "CBF index," which is % fast-wave component of EEG divided by AVDO2, was similar to that of CBF. Barbiturates reduced CMRO2 and fast-wave component during administration, possibly improving the relatively hypermetabolic state, and reduced the mortality rate to 0%. The maximum effects of barbiturate could be expected by administering the drug at the stage of delayed hypoperfusion with relative hypermetabolism, indicated by rapid recovery of the % fast-wave component, high AVDO2, and low CBF index.

Animals↗