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PubMed1966

Toxicological statistics for barbiturates, other sedatives, and tranquillizers in Ontario: a 10-year survey.

A steady increase in the number of cases of poisoning due to barbiturates, tranquillizers and non-barbiturate sedatives has been noted for Ontario by the Attorney-General's Laboratory, Toronto, during the period 1955-1964 on the basis of submitted material. Five cases of poisoning by barbiturates were recorded in 1955 and 193 in 1964.Urine and blood samples from persons charged with driving motor vehicles while under the influence of drugs were also examined. In 1958 only one such case was reported to the Laboratory, whereas 25 cases were recorded in 1964; barbiturates were detected in 18 of these 25. Patients must be warned of the risks of ingesting alcohol while receiving barbiturate treatment.

Automobile Driving↗
PubMed1984

Effects of barbiturates, phencyclidine, ketamine and analogs on cerebral circulation and cerebrovascular muscle.

Although barbiturates are often effective as therapeutic agents in several types of brain ischemia, there is no consensus as to their mechanisms of action. Exactly why other intravenous anesthetics such as ketamine are not effective therapies in brain ischemia is not known. Structural analogs of ketamine such as phencyclidine (PCP) not only exert potent hallucinogenic properties and are widely abused drugs, but often result in hypertensive encephalopathies and death. In view of the paucity of information on the cerebral circulatory actions of barbiturates, ketamine and PCP (and analogs), in-vivo (microcirculatory) and in-vitro studies were undertaken. Barbiturates, in anesthetic concentrations (e.g., 10(-5) to 10(-4) M), were found to exert direct vasodilator actions on cerebral arterial smooth muscle; these relaxant actions appear to be related to inhibition of calcium ion (Ca2+) influx in cerebral vessels. The latter may be important in the salutory actions of barbiturates in brain ischemia, head trauma and cerebrovasospasm. Unlike barbiturates, ketamine was found to exert spasmogenic actions on cerebral arteries, which may aid in explaining the inability of this anesthetic to be of therapeutic value in brain ischemia. PCP and its analogs, as well as other hallucinogenic molecules (e.g., LSD, mescaline) produced spasms in cerebral arterioles, venules and arteries in concentrations which mimic their hallucinogenic potencies. Distinct PCP-like receptors which subserve contraction appear to exist on large as well as microscopic cerebral blood vessels. Spasms induced by PCP, its analogs and ketamine can be readily reversed or prevented completely by calcium channel blockers. The latter agents could be quite useful, clinically, in prevention of cerebral infarction, hypertension and fatality associated with PCP (and analogs) intoxication.

Barbiturates↗
PubMed1978

Detection of barbiturates by latex agglutination inhibition.

A latex-agglutination inhibition test was developed and evaluated for the detection of barbiturates, primarily in urine, but it has applicability to serum. The 2-h test was performed with samples free of gross debris in a 37 degree C heat block and the reaction between the barbiturate antibody and the barbiturate-latex, at pH 7.3, was inhibited by urines containing secobarbital, amobarbital, pentobarbital, butabarbital, or phenobarbital. For laboratory standards the test was particularly sensitive to secobarbital (300 microgram/litre) and relatively insensitive to amobarbital (5000 microgram/litre). In clinical specimens some barbiturates were detected at levels as low as 150 microgram/litre. The test was specific, and negative endpoints were frequently noted in as little as 30 min. The effects of variables (antiserum dilution, urine specific gravity, heat block temperature, sample size, and type of barbiturate) on the degree of agglutination were also determined.

Agglutination Tests↗
PubMedDate not supplied

Relationship between lipophilicity and hepatic dispersion and distribution for a homologous series of barbiturates in the isolated perfused in situ rat liver.

The hepatic disposition kinetics of a homologous series of 5-n-alkyl-5-ethyl barbituric acids (methyl, ethyl, propyl, butyl, and pentyl) were determined using a single-pass perfused in situ rat liver preparation. The perfusion experiments were conducted using protein-free Krebs bicarbonate medium, delivered at a constant flow of 15 ml/min. Each barbiturate was injected separately into the portal vein as a rapid bolus (25 micrograms/50 microliters) at appropriate intervals in a random order. The venous outflow concentrations of the barbiturates were determined by HPLC. A nonlinear least squares program was used to fit the axial dispersion model of hepatic elimination to the outflow profiles. With increasing length of the alkyl chain, there was a significant increase in the volume of distribution in the liver (0.85 +/- 0.12 ml/g for methyl and 4.87 +/- 1.27 ml/g for pentyl), which led to an increased organ mean transit time (35 +/- 2.4 sec for methyl and 223 +/- 32.8 sec for pentyl). The increased volume of distribution may have arisen from greater binding to intracellular proteins and/or greater partitioning into lipophilic components of hepatic tissue. The dispersion numbers of this homologous series, a measurement of relative axial spreading, were similar (0.28-0.39), despite the wide range of log P values (0.02-2.23) among them. The similarity between the dispersion number for each barbiturate and that for reference markers (erythrocytes, albumin, and water) suggests that the relative axial spreading of these barbiturates is determined primarily by the heterogeneity of the hepatic vasculatory system.

Animals↗
PubMedDate not supplied

Interaction of hydralazine with barbiturates.

Barbiturates given together with hydralazine significantly change the hypotensive effect of the latter. The final effect depends on the kind of barbiturate, time of its administration, and initial functional state of the circulatory system. Hydralazine given together with barbiturates significantly prolongs their hypnotic action and shortens the latency of that action. In the case of a short-acting barbiturate, hexobarbital, this effect appears in normotensive rats only if the barbiturate is given 60 min prior to hydralazine administration.

Animals↗
PubMed1997

Experimental studies on effects of barbiturate on electroencephalogram and auditory brain-stem responses.

The effects of pentobarbital on electroencephalogram (EEG) and auditory brain-stem response (ABR) were evaluated in 13 Japanese white male rabbits, divided into two groups, 7 and 6, respectively. After baseline evoked responses were obtained, pentobarbital was infused intravenously at 60 mg/kg/h in both groups. EEGs and ABR were recorded with 15 min intervals. When the blood concentration of pentobarbital reached therapeutic levels (2.0-5.0 mg/dL), cortical and hippocampal EEGs became isoelectric. Although the appearance of ABR waves was significantly delayed, each wave was clearly observed in spite of isoelectric EEG levels. The rabbits in one group were killed at that time, and their brains were removed to determine the concentration of pentobarbital in the brain tissue. In another group, pentobarbital was additionally infused at the rate of 120 mg/kg/h. Although the waves (II-IV) of the ABR gradually disappeared with increasing dosage, wave I was present until just prior to cardiac arrest. It is considered that the persistency of ABR at high doses of barbiturates is characteristic of patients in deep barbiturate coma. Therefore, at the diagnosis of brain death, there is no necessity to consider the half-life of the barbiturate, even if an excessive amount of barbiturate remains in the brain. In this study, pentobarbital concentration in the brain was nearly equal to the concentration in the blood. However, it is estimated that a large amount of barbiturate is accumulated in the brain of a patient after brain death because the blood flow in the brain is stagnant.

Animals↗
PubMed1977

Effects of diazepines and barbiturates on hippocampal recurrent inhibition.

The effects of two diazepines (diazepam and Ro 11-7800) and 3 barbiturates (thiamylal, pentobarbitol and phenobarbital) on GABA-mediated recurrent inhibition were assessed on single hippocampal pyramidal cells and on population spikes using extracellular recording techniques. Recurrent inhibition was evoked in spontaneously active CA1 pyramidal cells by stimulation of the fimbria or the alveus with single shocks. Microiontophoretic application of Ro 11-7800 or systemic application of diazepines or barbiturates resulted in an increase of the duration of the inhibition and in a concomitant depression of the spontaneous firing in most neurones tested. When the firing rates were kept constant artificially, using excitant amino acids, a prolongation of the recurrent inhibition was observed with barbiturates but not with diazepines. The duration of the inhibition, which was assessed from CA1 population spikes elicited by double shocks to the fimbria, was prolonged following systemic application of diazepines or barbiturates. It is concluded that both diazepines and barbiturates are able to potentiate GABAergic recurrent inhibition in the hippocampus. The demonstration of this effect appears to depend critically on certain experimental conditions.

Animals↗
PubMed1982

The effects of ketamine HCl and barbiturate anaesthesia on the metabolic clearance and production rates of testosterone in the male rhesus monkey, Macaca mulatta.

The study compares metabolic clearance rates, production rates and serum levels of testosterone in conscious and ketamine and barbiturate anaesthetized adult male rhesus monkeys. Using the single injection technique for the determination of metabolic clearance rate, a significant increase in metabolic clearance rate from 430 +/- 71 l/day in conscious animals to 908 +/- 46 l/day for ketamine and 1224 +/- 174 1/day for barbiturate anesthetized animals was observed. Serum testosterone was increased from 106 +/- 9 ng/100 ml to 450 +/- 186 ng/100 ml in barbiturate anaesthetized animals, and this marked increase in serum testosterone was accompanied by a 13-fold increase in the production rate of testosterone from 0.44 +/- 0.04 mg/day to 6.0 +/0 3.3 mg/day. Serum testosterone levels and production rates were not significantly different in conscious and ketamine anaesthetized animals. Barbiturate anaesthesia caused continual changes in serum LH and testosterone levels over an observation period of 3.5 h. Serum LH gradually increased from 4.8 +/- 2.1 mIU/ml to 19.0 +/- 4.1 mIU/ml within 1 h, while serum testosterone rose from 214 +/- 63 ng/100 ml to 836 +/- 53 ng/100 ml within 2 h. In the light of these findings it may be concluded that barbiturate anaesthesia is not suitable for such prolonged studies of endocrine function. Effects exerted by ketamine anaesthesia are less pronounced.

Animals↗
PubMed1983

Effects of barbiturates and ethanol on muscimol-induced release of [3H]-D-aspartate from rodent cerebellum.

The K+-stimulated release of [3H]-D-aspartate and [14C]-GABA from synaptosomal (P2) fractions prepared from rat cerebellum was studied. Muscimol enhanced the release of [3H]-D-aspartate by 60-75% and the release of [14C]-GABA by 20-35%. Muscimol also enhanced the release of [3H]-D-aspartate from P2 fractions prepared from swine and mouse cerebellum. Pentobarbital, an anesthetic barbiturate, had no effect on basal or K+-stimulated release of [3H]-D-aspartate or [14C]-GABA but potentiated the enhancement of [3H]-D-aspartate release by muscimol. The EC50 was approx. 50 microM. The S(-)-isomer of pentobarbital was more potent than the R(+)-isomer in potentiating the action of muscimol, in agreement with the anesthetic potencies of the isomers. Phenobarbital, an anticonvulsant barbiturate, enhanced release of [3H]-D-aspartate and [14C]-GABA in the absence of muscimol. In contrast, the convulsant barbiturate 5-ethyl-5-(2'-cyclohexylidene-ethyl)barbituric acid (CHEB) caused a significant increase in basal release of [3H]-D-aspartate and [14C]-GABA in the absence of muscimol. Diazepam and ethanol had no effect on the release of [3H]-D-aspartate and did not potentiate the action of muscimol. These experiments provide biochemical evidence for an enhancement of the action of GABA by anesthetic barbiturates. This effect appears to be mediated through a benzodiazepine-insensitive presynaptic GABA receptor.

Animals↗
PubMed1979

Barbiturate tolerance and hypersensitivity of arterial smooth muscle.

Experiments were undertaken on rats chronically treated with pentobarbital sodium, 50 mg/kg three times per day for a period of five days, to determine whether excised aortic or venous (portal vein) smooth muscle would demonstrate any change in reactivity to catecholamines or potassium chloride. Although sleeping time was reduced 50% (indicative of tolerance to the barbiturate), mean arterial blood pressure was not affected. Aortic strips, but not portal veins, excised from barbiturate-treated animals exhibited hypersensitivity to both contractile stimulants. Potassium-depolarized calcium-depleted aortic tissue, but not portal venous smooth muscle, from the barbiturate-treated animals contracted to lower concentrations of Ca2+ than did the arterial smooth muscle from the saline-treated control rats. The present observations thus indicate that chronic barbiturate treatment in rats can induce drug supersensitivity of excitable tissue other than one associated with the central nervous system. Our results on arterial smooth muscle could help to shed light on the unexplained rises in arterial blood pressure observed in humans undergoing barbiturate withdrawal.

Animals↗
PubMed2000

Results of barbiturate antiepileptic drug discontinuation on antipsychotic medication dose in individuals with intellectual disability.

Five individuals with intellectual disability prescribed both a barbiturate antiepileptic drug (AED) and an antipsychotic medication were identified in a public residential facility. It was hypothesized that antipsychotic medication was prescribed at doses higher than necessary as a result of inadvertent barbiturate AED behavioural side-effects thought to be part of the underlying psychiatric or behavioural condition. To test this hypothesis, barbiturate AEDs were gradually reduced, and replaced with either carbamazepine or valproic acid, and antipsychotic medication was gradually reduced as well. Challenging behaviours, such as physical aggression, self-injurious behaviour and property destruction, were measured with a frequency count or partial interval recording, and retrospectively analysed for time periods of approximately 60 days before phenobarbital reduction, after phenobarbital discontinuation and after the lowest antipsychotic medication dose. Challenging behaviour collectively decreased by 81.5% after barbiturate discontinuation, mean antipsychotic medication dose significantly decreased from 146 mg day(-1) (SD = 98) to 106 mg day(-1) (SD = 88) chlorpromazine equivalence, and antipsychotic medication was discontinued in the cases of two individuals. Compared to the prebarbiturate AED reduction period, challenging behaviour collectively decreased by 96.3% after the lowest antipsychotic medication dose, which confirmed that reduced antipsychotic medication was not achieved at the expense of behaviour deterioration. The data supported the hypothesis that discontinuation of barbiturate AEDs results in decreased challenging behaviour and less antipsychotic medication.

Adult↗
PubMed1983

[Barbiturate therapy in neurosurgery].

Thirty patients with an acute midbrain syndrome were treated by high dose barbiturate therapy. Of these patients 19 had a severe head injury. In 8 patients the symptoms of acute midbrain syndrome developed after subarachnoid haemorrhage. In three patients these symptoms were caused by postoperative swelling or ischaemia. The results of those patients, who were treated with barbiturates after head injury were much better than in 16 other patients, who had no barbiturates. The indications for high dose barbiturate therapy in neurosurgery are discussed with reference to other publications and to the pathophysiological effects of barbiturates.

Adolescent↗
PubMed1992

Propofol and barbiturate depression of spinal nociceptive neurotransmission.

Barbiturates are often described as non-analgesic or even hyperalgesic agents; the newer intravenous anesthetic agent propofol is said to be non-analgesic. Both propofol and barbiturates occupy sites on the GABAA receptor. The present study was designed to compare the effects of propofol and barbiturates on nociceptive-related neurotransmission in neonatal rat spinal cord; to search for actions that might be hyperalgesic; and to determine the extent to which propofol depression of nociceptive neurotransmission is mediated by GABAA receptors. The monosynaptic reflex, a slow ventral root potential (slow VRP) and the dorsal root potential (DRP) were recorded from isolated neonatal (1-5 days old) superfused rat spinal cords in response to electrical stimulation of a lumbar dorsal root. The slow VRP and the DRP are related to nociception. Propofol (0.5-10 microM), pentobarbital (1-10 microM), and thiopental (1-10 microM) reversibly depressed the slow VRP. Dose-response curves were monophasic and linear over this range. The monosynaptic reflex was unaffected. The GABAA agonist muscimol (0.2-1 microM) also depressed the slow VRP. Propofol and barbiturate slow VRP depression was antagonized by the GABAA antagonist bicuculline (1 microM). Propofol depressed the response evoked by direct application of substance P. The DRP is a GABAA-mediated depolarization of primary afferent nerve terminals that diminishes the effectiveness of nociceptive input. Propofol and thiopental increased electrically evoked DRP amplitude and increased the DRP evoked by application of muscimol. Both propofol and barbiturates thus depressed the nociceptive-related slow VRP and enhanced the antinociceptive DRP; their effective concentrations are at or close to the general anesthetic range for these agents. No anti-analgesic or hyperalgesic effect was observed. (ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1999

Comparison of the effects of convulsant and depressant barbiturate stereoisomers on AMPA-type glutamate receptors.

BACKGROUND: Alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA)-type glutamate receptors mediate fast excitatory synaptic transmission in the central nervous system. Although barbiturates have been shown to suppress the AMPA receptor-mediated responses, it is unclear whether this effect contributes to the anesthetic action of barbiturates. The authors compared the effects of depressant [R(-)] and convulsant [S(+)] stereoisomers of 1-methyl-5-phenyl-5-propyl barbituric acid (MPPB) on the AMPA and gamma-aminobutyric acid type A (GABA(A)) receptor-mediated currents to determine if the inhibitory effects on AMPA receptors correlate to the in vivo effects of the isomers. METHOD: The authors measured whole-cell currents in the rat cultured cortical neuron at holding potential of -60 mV. Kainate 500 microM was applied as the agonist for AMPA receptors. Thiopental (3-300 microM), R(-)-MPPB or S(+)-MPPB (100-1,000 microM) was coapplied with kainate under the condition in which the GABA(A) receptor-mediated current was blocked. Effects of MPPB isomers on the current elicited by GABA 1 microM were studied in the separate experiments. RESULTS: Thiopental inhibited the kainate-induced current reversibly and in a dose-dependent manner, with a concentration for 50% inhibition of 49.3 microM. Both R(-)-MPPB and S(+)-MPPB inhibited the kainate-induced current with a little stereoselectivity. R(-)-MPPB was slightly but significantly more potent than S(+)-MPPB. In contrast, R(-)-MPPB enhanced but S(+)-MPPB reduced the GABA-induced current. CONCLUSIONS: Both convulsant and depressant stereoisomers of the barbiturate inhibited the AMPA receptor-mediated current despite of their opposite effects on the central nervous system in vivo. Although thiopental exhibited a considerable inhibition of AMPA receptors, the results suggest that the inhibition of AMPA receptors contributes little to the hypnotic action of the barbiturates.

Animals↗
PubMed2006

Dose-dependent influence of barbiturates but not of propofol on human leukocyte phagocytosis of viable Staphylococcus aureus.

OBJECTIVE: Deep sedation with barbiturates or propofol is a standard therapy for patients with critically elevated intracranial pressure. Such patients are prone to infectious complications, especially to pneumonias, which are most commonly caused by Staphylococcus aureus. Although various immunomodulatory effects of barbiturates have been described in vitro, their influence on the phagocytosis of viable S. aureus has yet to be investigated. Therefore, we examined the effects of thiopentone, methohexitone, and propofol on the phagocytosis of viable S. aureus. DESIGN: Laboratory study. SETTING: University laboratory. PATIENTS: Ten healthy volunteers aged 32.5 +/- 7 yrs. INTERVENTIONS: Blood sampling. MEASUREMENTS AND MAIN RESULTS: Whole blood samples were preincubated with different concentrations of thiopentone, methohexitone, and propofol, which is an isopropylphenol derivate. After viable S. aureus was added, phagocytosis was stopped at different time points. Leukocytes were then stained with monoclonal antibodies for flow cytometric analysis of granulocyte recruitment (ratio of ingesting granulocytes) and phagocytosis activity (fluorescence intensity of ingested bacteria). Both barbiturates inhibited granulocyte recruitment and phagocytosis activity in a dose-dependent manner, whereas propofol did not affect any of the investigated variables. At concentrations higher than 7.6 x 10(-3) M (for thiopentone, p < .008) and 1.1 x 10(-3) M (for methohexitone, p < .04), granulocyte recruitment and phagocytosis activity were significantly inhibited. The calculated inhibitory concentrations (IC50) of thiopentone for granulocyte recruitment and for phagocytosis activity were 1.3 x 10(-2) M and 1.1 x 10(-2) M, respectively. The corresponding values for methohexitone were 3.6 x 10(-3) M and 1.1 x 10(-3) M. CONCLUSIONS: Our in vitro model points at substantially different effects of barbiturates and propofol on phagocytosis of S. aureus, which is one of the most important pathogens in patients who need neuroprotective therapy. The inhibitory effects of both barbiturates demonstrate a strong dose-dependency, with more pronounced effects for methohexitone. Impairment of phagocytosis activity was more pronounced than granulocyte recruitment.

Adult↗
PubMed1996

Direct activation of GABAA receptors by barbiturates in cultured rat hippocampal neurons.

1. The direct activation of the GABAA receptor by pentobarbitone (PB) and phenobarbitone (PHB) was characterized in cultured rat hippocampal neurons using whole-cell voltage clamp and single channel recording techniques. 2. In whole-cell recordings, PB and PHB produced a concentration-dependent activation of Cl- current (EC50 values, 0.33 and 3.0 mM, respectively). The response to the barbiturates was similar to that produced by GABA, although GABA was more potent (EC50, 5.5 microM). PB and PHB were substantially more potent in enhancing the response to 1 microM GABA (EC50 values, 94 microM and 0.89 mM, respectively). The maximal magnitude of the responses to PB was similar to that of the maximal response to GABA or GABA + PB. PHB appeared to be modestly less efficacious. 3. The mean deactivation time constant for whole-cell Cl- currents evoked by 1 mM PB + 1 microM GABA was significantly longer (480 +/- 34 ms) than for 1 mM PB (170 +/- 9 ms) or 1 microM GABA (180 +/- 14 ms) alone. 4. Whole-cell currents directly activated by 300 microM PB and 1 microM GABA were blocked by the GABA receptor antagonists bicuculline and picrotoxin. 5. Unitary GABAA receptor channel currents evoked by 300 microM PB had similar main conductance, mean open time and mean burst duration as those activated by 2 microM GABA alone. Single channel openings and bursts were of shorter mean duration when 100 and 300 microM PHB were used. 6. High concentrations of PB (1-3 mM) and PHB (3-10 mM) produced a rapid block of currents activated by the barbiturate alone or by the barbiturate in the presence of 1 microM GABA. The estimated IC50 values for block of PB- and PHB-potentiated GABA currents were 2.8 and 12.9 mM, respectively. 7. Single channel currents activated by high concentrations of PB and PHB alone or in the presence of GABA demonstrated flickering, probably reflecting fast channel block. 8. We conclude that the gating of the GABAA receptor channel by PHB and PB is functionally similar to that produced by the natural agonist GABA alone, but distinct from that obtained when barbiturates modulate the response to GABA. At high concentrations, the barbiturates produce a channel blocking action that limits the maximum total current conducted by the channel.

Animals↗
PubMed1988

Barbiturate anesthesia in the treatment of status epilepticus: clinical experience with 14 patients.

We report our experience using barbiturate anesthesia for the treatment of refractory status epilepticus. Following a retrospective review of eight patients treated with a variety of barbiturates and dosing regimens, we established a specific protocol employing pentobarbital and evaluated it prospectively in six patients. Among the 14 patients, intravenous barbiturates, when administered with a loading dose followed by continuous infusion, were uniformly effective in aborting seizures and producing a burst-suppression EEG pattern. Other than the pupillary light reflex, most patients lost all brainstem reflexes and motor responses during therapy. Barbiturate-induced hypotension was observed in 9 of the 14 patients, and required treatment with pressors in seven cases. Three patients died early as a consequence of their underlying illness, while three others died late for reasons unrelated to the status itself or to anticonvulsant therapy. The time to recovery of function following anesthesia varied highly, spanning hours to days for return of motor function and days to weeks for cognition. Of the eight survivors, four were left with mild cognitive deficits, one returned to his baseline dementia, and three had residual encephalopathies (severe in two). We conclude that barbiturate anesthesia is an extremely effective therapy for refractory seizures. However, its use necessitates recognition of untoward cardiovascular responses and prolonged intensive care.

Anesthesia↗
PubMedDate not supplied

The effects of high-dose barbiturates on the acoustic reflex and auditory evoked responses. Two case reports.

The effects of high-dose barbiturates (pentobarbital) on the acoustic reflex, and the auditory brainstem (ABR) and middle-latency (AMR) responses, are illustrated with two case reports. Auditory electrophysiologic data were recorded serially during recovery from therapeutic barbiturate coma. ABR latency remained within normal limits in barbiturate coma, but amplitude of the wave I component was abnormally augmented. Contralateral and ipsilateral acoustic reflex activity, and the Pa component of the AMR, were not observed in barbiturate coma, and reappeared with the emergence of brainstem neurologic signs. These findings suggest a fundamental difference in the neurophysiologic substrate of the ABR vs. acoustic reflex and AMR. Possible mechanisms for the differential influence of barbiturates on these three auditory electrophysiologic measures are offered.

Adolescent↗