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PubMed1981

Barbiturates: active form and site of action at node of Ranvier sodium channels.

Barbiturate sodium channel block was investigated in the voltage-clamped amphibian node of Ranvier. Internal pH was manipulated by diffusion of buffers from the cut internodes. Like local anesthetics and volatile general anesthetics, barbiturates shift the voltage dependence of inactivation in the hyperpolarizing direction. A barbiturate anion, 5-phenyl barbituric acid, blocks sodium channels when applied externally or internally. On external application, block is of very slow onset. The barbiturate anion, like the local anesthetic cation, thus appears to bind to a receptor site on the axoplasmic side of the membrane. Unlike local anesthetics, however, phenobarbital exerts a frequency-dependent block which is modified by changes in internal pH and is not affected by changes in external pH. In addition, barbiturate frequency dependence is apparently more exclusively involved with channel inactivation. The results suggest a barbiturate sodium channel binding site closer to the axoplasm than the local anesthetic binding site is and also suggest that there is a proton barrier between the two sites.

Animals↗
PubMed1981

Barbiturate-induced coma to protect against cerebral ischemia and increased intracranial pressure.

The use of barbiturates to induce coma as a means of extending the period of reversible cerebral ischemia is reviewed. Barbiturate use in patients who had had strokes or were undergoing aneurysm surgery was initially encouraging. In uncontrolled feasibility trials in patients with cardiopulmonary arrest or in deep coma, 40 patients received 10 mg/kg thiopental sodium by i.v. push followed by 20 mg/kg thiopental sodium i.v. over the next 30 minutes; 60% of these patients regained consciousness. In a subgroup of 22 patients who had ischemia normally associated with a 90% mortality rate, 14 recovered completely. In the largest clinical trial, 45 patients with severe head injury and elevated intracranial pressure received 3--5 mg/kg pentobarbital over 10--20 minutes. A serum barbiturate level of 2.5--4.0 mg/dl was maintained for 14 days, and 30% of these patients recovered but with neurologic deficits. Other results in stroke and drowning victims were not as encouraging. It is concluded that barbiturate therapy is beneficial in the lowering of intracranial pressure. Focal and global cerebral ischemia have been shown amenable to barbiturate therapy in isolated cases. The prophylactic use of barbiturates in surgical procedures requiring focal cerebral anoxia appears to be beneficial. Controlled trials of the use of barbiturate-induced coma are clearly indicated.

Animals↗
PubMed1980

Effect of the CURB campaign on barbiturate prescribing in Northern Ireland.

Barbiturate prescribing in general practice in Northern Ireland was monitored from computer data on prescription pricing for the years 1966 to 1979, and subjected to two methods of statistical analysis.Over the last decade a very marked decline in the prescribing of barbiturate hypnotics was accompanied by progressive decreases in barbiturate anti-epileptic and combination product utilization. During the 1975 to 1977 CURB campaign there was a statistically significant greater decrease in the total quantity of barbiturate hypnotics prescribed, but the downward trend in the numbers of prescriptions written was not significantly greater than before the campaign. The main effect of CURB, therefore, was to reduce the average quantity of barbiturate per prescription. The changes in barbiturate combination product prescribing between the CURB years were consistently large, whilst anti-epileptic barbiturate prescribing decreased less significantly towards the end of the campaign.

Barbiturates↗
PubMed1992

Experimental study on the indications for barbiturate therapy. Change in haemodynamics and the influence of dopamine.

The effect of barbiturates on the cerebral haemodynamics and the influence of dopamine on barbiturates were investigated using 20 cats, and clinical indication of barbiturate therapy is discussed. Cerebral blood flow, oxygen extraction fraction, and cerebro-vascular resistance as well as physiological variables were evaluated at various concentrations of barbiturates in the blood. Thiamylal caused simultaneous reduction of mean arterial blood pressure and cerebral blood flow. As the disruption of autoregulation proceeded, cerebro-vascular resistance and oxygen extraction fraction increased till the barbiturate-induced coma stage. Furthermore, cerebro-vascular resistance increased much more markedly by the combined use of dopamine. Clinically, our results indicate barbiturates would increase cerebral circulatory disturbances caused by vasospasm following subarachnoid haemorrhage because barbiturates further increase cerebro-vascular resistance. Then again, the combined use of dopamine is not preferable because of deterioration in vasospasm.

Animals↗
PubMed1990

Physiological modulation of the GABA receptor by convulsant and anticonvulsant barbiturates in cultured rat hippocampal neurons.

The actions of convulsant and sedative barbiturates on responses to gamma-aminobutyric acid (GABA) application and on inhibitory postsynaptic currents were compared using voltage-clamp techniques in cultured rat hippocampal neurons. The convulsant barbiturates, 5-ethyl-5-(3-methylbut-2-enyl) barbituric acid (3M2B), and (+)-5-ethyl-5-(1,3-dimethylbutyl) barbituric acid [+)-DMBB), and the sedative barbiturate, 5-ethyl-5-(3-methylbutyl) barbituric acid (3MB), all potentiated GABA-mediated chloride currents. In addition, these compounds prolonged the duration of GABAergic inhibitory postsynaptic currents. The similarity between the action of convulsant and sedative barbiturates suggests that the convulsant activity of 3M2B and (+)-DMBB are not mediated by their actions at GABAergic synapses.

Animals↗
PubMed1995

Barbiturates inhibit hexose transport in cultured mammalian cells and human erythrocytes and interact directly with purified GLUT-1.

Barbiturates reduce cerebral blood flow, metabolism, and Glc transfer across the blood-brain barrier. The effect of barbiturates on hexose transport in cultured mammalian cell lines and human erythrocytes was studied. Pentobarbital inhibits [3H]-2-dGlc uptake in 3T3-C2 murine fibroblasts by approximately 95% and approximately 50% at 10 and 0.5 mM, respectively. Uptake of [3H]-2-dGlc is linear with time in the presence or absence of pentobarbital, and the percent inhibition is constant. This suggests that hexose transport, not phosphorylation, is inhibited by barbiturates. Inhibition by pentobarbital of hexose transport in 3T3-C2 cells is rapid (< 1 min), is not readily reversible, is not altered by the presence of albumin [1% (w/v)], and is independent of temperature (4-37 degrees C) and the level of cell surface GLUT-1. The IC50's for inhibition of hexose transport in 3T3-C2 cells by pentobarbital, thiobutabarbital, and barbital are 0.8, 1.0, and 4 mM, respectively. This is consistent with both the Meyer-Overton rule and the pharmacology of barbiturates. Neither halothane (< or = 10 mM) nor ethanol [< or = 0.4% (v/v)] significantly inhibits hexose transport. Inhibition by pentobarbital (0.5 mM) of [3H]-2-dGlc uptake by 3T3-C2 cells decreases the apparent Vmax (approximately 50%) but does not alter the apparent Km (approximately 0.5 mM). Inhibition of hexose transport by barbiturates, but not ethanol [< or = 0.4% (v/v)], is also observed in human erythrocytes and four other cultured mammalian cell lines. Pentobarbital quenches (Qmax approximately 75%) the intrinsic fluorescence of purified and reconstituted GLUT-1 (Kd approximately 3 mM). Quenching is independent of Glc occupancy, is unchanged by mild proteolytic inactivation, and does not appear to directly involve perturbations of the lipid bilayer. We propose that barbiturates can interact directly with GLUT-1 and inhibit the intrinsic activity of the carrier. Glc crosses the blood-brain barrier primarily via the GLUT-1 of the endothelial cells of cerebral capillaries. Partial inhibition of this process by barbiturates may be of significance to cerebral protection.

3T3 Cells↗
PubMed1993

Barbiturates and hyperventilation during intracranial hypertension.

OBJECTIVE: The purpose of this study was to determine the effect of hyperventilation alone and hyperventilation plus barbiturate therapy on intracranial pressure, global and regional cerebral blood flow rates, cerebrovascular resistance, and cerebral perfusion pressure in adult dogs with and without intracranial hypertension induced by epidural balloon. DESIGN: Prospective, randomized, controlled study. SETTING: An animal laboratory of a university hospital. Four sequential global and regional cerebral blood flow determinations were made in each animal during monitoring of heart rate and systemic arterial pressure, during respiratory control and arterial blood gas monitoring, intracranial pressure monitoring, and with or without inflation of an epidural balloon catheter. SUBJECTS: Acute mongrel dogs obtained from the Baylor Center for Comparative Medicine. Five groups of animals were studied. In group 1, the response to hyperventilation was assessed in dogs without increased intracranial pressure. In group 2, the response to hyperventilation was assessed in animals with acute intracranial hypertension. In group 3, the response to hyperventilation plus barbiturate therapy was assessed in dogs without increased intracranial pressure. In group 4, the response to hyperventilation plus barbiturate therapy was assessed in dogs with acute increased intracranial pressure. In group 5, a group of dogs with increased intracranial pressure was treated with neither hyperventilation nor barbiturates. INTERVENTIONS: Hyperventilation, hyperventilation plus barbiturate therapy, or no interventions were studied in these experimental paradigms. MEASUREMENTS AND MAIN RESULTS: The main outcome measures were changes in intracranial pressure and/or changes in regional or total cerebral blood flow. A significant decrease in intracranial pressure and cerebral blood flow rate was produced by hyperventilation alone in groups with intracranial hypertension. Combined hyperventilation and barbiturate therapy resulted in a significant further decrease in cerebral blood flow rate in animals with normal and increased intracranial pressure, but no greater decrease in intracranial pressure was seen compared with treatment with hyperventilation alone. Cerebral perfusion pressures remained normal despite significant decreases in cerebral blood flow rates. CONCLUSIONS: These studies suggest that barbiturate administration in this model of intracranial hypertension was no more effective in reducing increased intracranial pressure than hyperventilation alone.

Acute Disease↗
PubMed1989

Barbiturate regulation of kinetic properties of the GABAA receptor channel of mouse spinal neurones in culture.

1. Barbiturate regulation of the kinetic properties of gamma-aminobutyric acidA (GABA) receptor channel chloride currents from somata of mouse spinal cord neurones were investigated using whole-cell and excised outside-out patch-clamp recording techniques. 2. GABA (2 microM), GABA (2 microM) plus phenobarbitone (PhB) (500 microM) and GABA (2 microM) plus pentobarbitone (PB) (50 microM), applied by pressure ejection from blunt perfusion micropipettes, evoked inward chloride currents when neurones or patches were voltage clamped at -75 mV and the chloride equilibrium potential was 0 mV. GABA receptor channel currents were increased by PhB and PB. 3. Single GABA receptor channel currents were recorded with a main conductance state of 27 pS and a less frequent subconductance state of 16.5 pS. The conductances of the two states were unchanged by the barbiturates. 4. The main conductance state kinetics were analysed. GABA alone or with the barbiturates gated the channel open singly and in groups of openings. 5. The barbiturates increased GABA receptor channel mean open time and shifted frequency histograms of channel open times to longer times. 6. Three exponential functions were required to fit the frequency histograms of GABA receptor channel open times, suggesting that the channel has at least three open states (O1, O2, O3). The time constants for the exponential functions (0.9, 2.7 and 7.8 ms, respectively) were unchanged by the barbiturates. The increases in mean open times and the shifts of the open-time frequency histograms by the barbiturates were due to a reduction in relative frequency of occurrence of the two short open states (O1 and O2) and to an increase in the relative frequency of occurrence of the longest open state (O3). 7. Frequency histograms of GABA receptor channel closed times were fitted with five exponential functions, suggesting that the channel has multiple closed states. None of the time constants nor areas of the exponential functions were significantly changed by the barbiturates. 8. For analysis, a burst was defined as openings surrounded by closures greater than a critical closed time, tc, of 5 ms. For GABA (2 microM), frequency histograms of GABA receptor channel bursts were fitted with three exponential functions, suggesting that the channel has three burst states (B1, B2, B3). The B1 burst state was probably a single opening to the O1 open state while the B2 and B3 burst states were probably composed of multiple openings to the O2 and O3 open states.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1994

Effect of anesthetic and convulsant barbiturates on N-methyl-D-aspartate receptor-mediated calcium flux in brain membrane vesicles.

The effects of anesthetic and convulsant barbiturates on brain N-methyl-D-aspartate (NMDA) receptor function were examined in a cell-free membrane vesicle preparation from mouse hippocampus. Increases in intracellular free calcium concentrations (Cai) were determined using a fluorescent dye, Indo-1, after stimulation with the NMDA receptor agonist, L-glutamate. Anesthetic barbiturates inhibited NMDA responses in a concentration-dependent manner with a rank order of potency of secobarbital > amobarbital > pentobarbital > mephobarbital = phenobarbital >> barbital. However, the IC50 values for these barbiturates were larger than probable blood anesthetic concentrations. Barbiturates with both anesthetic and convulsant effects in mice [optical isomers of pentobarbital and secobarbital, 5-(2-cyclohexylideneethyl)-5-ethylbarbituric acid and (+/-)-dimethylbutylbarbituric acid] also reduced NMDA responses. Inhibition of NMDA responses by racemic pentobarbital or isomers of pentobarbital was noncompetitive. Resting Cai was altered by all barbiturates tested except secobarbital and barbital, but not in a consistent manner, suggesting that the effect of barbiturates on resting Cai is not related either to their effects on NMDA receptor responses or to their behavioral effects. These results show that anesthetic and convulsant barbiturates inhibit NMDA responses, but their anesthetic and convulsant activities may be primarily due to their effects on other brain targets.

Animals↗
PubMed1981

Barbiturate effects on acute experimental intracranial hypertension.

Acute intracranial hypertension was induced in cats by progressive inflation of an epidural balloon. Changes in intracranial pressure (ICP), mean arterial pressure (MAP), cerebral perfusion pressure (CPP), heart rate (HR), electroencephalogram (EEG), and pupil size were studied in untreated animals and in animals that had received barbiturates at different stages during the experiment. In animals pretreated with barbiturates, the increase in ICP during balloon expansion was significantly less than in untreated animals (p less than 0.001). The CPP, initially higher in untreated animals, was not significantly different (P less than 0.05) as the mass lesion pressure-volume curve exceeded the inflection point. In the postdeflation period, the untreated animals developed a significant increase in ICP, whereas, in the barbiturate-pretreated group, the ICP returned to preinflation values, suggesting a protective effect of barbiturates against postcompression brain swelling. Barbiturates affected ICP and CPP differently in animals with intracranial hypertension due to the presence of an epidural balloon that was maintained inflated compared to those with postdeflation brain swelling. In the latter group, pentobarbital reduced ICP (p less than 0.05) without significantly decreasing the CPP, whereas, in the mass lesion group, barbiturates failed to reduce the ICP and caused a deterioration in CPP (p less than 0.025). Brain gross pathological changes were significantly less in the pretreated animals as compared with all other groups. The results suggest that if barbiturate treatment is to have therapeutic value, the timing of the therapy and the criteria for its initiation should be determined.

Animals↗
PubMed1979

High-dose barbiturate therapy in humans: a clinical review of 60 patients.

Over the past three years, high-dose barbiturate therapy has been used in the treatment of 60 patients with head injury (N = 45), encephalitis (N = 8), acute focal cerebral ischemia (stroke, N = 4), and global anoxia secondary to drowning (N = 3). High-dose barbiturates appear to be useful adjuncts in the control of intracranial hypertension refractory to other methods of therapy. Administration of barbiturates to patients with this problem will often reduce the requirement for osmotic agents, thereby facilitating medical management by avoiding hyperosmolality and fluid and electrolyte depletion. In a carefully controlled intensive care setting the risk of barbiturate therapy is low, though the costs and demands on personnel are great. Survival appeared to be improved in aptients with ,head injury and encephalitis. Although the ultimate outcome was not altered in patients with stroke or near-drowning, intracranial hypertension did not occur until barbiturate therapy was withdrawn. This experience provides an ethical basis to justify further randomized studies for determining whether or not barbiturates materially improve the neurological outcome following cerebral ischemic and traumatic insults.

Adolescent↗
PubMed1997

Barbiturate induced benzophenanthridine alkaloid formation proceeds by gene transcript accumulation in the California poppy.

Four barbiturates, barbituric acid, butethal, phenobarbital, and 2-thiobarbituric acid, of fourteen tested were found to induce accumulation of benzophenanthridine alkaloids in cell suspension cultures of the California poppy Eschscholzia california. When the plant cell suspension cultures were treated with 1 mM barbiturate, alkaloids accumulated to 100 mg/l within four days. This is a level comparable to that achieved with 300 microM concentration of the established secondary metabolite inducer methyl jasmonate. In contrast to methyl jasmonate, barbituric acid, and 2-thiobarbituric acid, butethal and phenobarbital treatment resulted in a different alkaloid profile, suggesting that only select cytochrome P-450 genes were activated by these latter two barbiturates. RNA gel blot analysis of barbiturate induced cell cultures confirmed that transcripts of at least two benzophenanthridine alkaloid biosynthetic genes cyp80b1 (encoding the cytochrome P-450-dependent monooxygenase (S)-N-methylcoclaurine 3'-hydroxylase) and bbe1 (encoding the covalently flavinylated berberine bridge enzyme) increased up to 5- to 7-fold over control values.

Alkaloids↗
PubMed1988

Acute barbiturate administration increases benzodiazepine receptor binding in vivo.

Barbiturates have been reported to augment benzodiazepine receptor affinity in vitro, but their effects in vivo are uncertain. We determined benzodiazepine receptor binding in vivo by specific uptake of [3H]Ro15-1788 after barbiturate administration. Pentobarbital (30 mg/kg) increased receptor binding in cerebral cortex and cerebellum at 30 min after injection, with a peak effect occurring at 1 h after dosage, and a return to control levels at 2 h. Specific binding was increased at 1 h after pentobarbital administration in a dose-dependent fashion (7.5-90 mg/kg). Pentobarbital at doses up to 30 mg/kg failed to alter nonspecific binding, but at doses of 60 mg/kg increases in nonspecific binding were observed. The increases in specific binding observed after barbiturate administration were most likely due to a change in apparent receptor affinity, as determined by administration of varying doses of clonazepam to pentobarbital-treated (30 mg/kg) animals. The order of potency of a series of barbiturates in augmenting benzodiazepine receptor binding in cerebral cortex and cerebellum in vivo was: secobarbital greater than pentobarbital greater than amobarbital greater than phenobarbital greater than barbital. The same relative rank order of potency exists for the anesthetic/hypnotic activity of these barbiturates. These data suggest that barbiturates increase the apparent affinity of benzodiazepine receptors in vivo; unlike their in vitro actions, these alterations can be detected with a receptor antagonist.

Animals↗
PubMed1984

Interaction of barbiturates with adenosine receptors in rat brain.

The effects of barbiturates on radioligand binding to inhibitory Ri adenosine receptors of rat brain membranes were investigated. Binding of the adenosine receptor agonist (-)N6-phenylisopropyl[3H]adenosine and the antagonist 1,3-diethyl-8-[3H]phenylxanthine was inhibited by several barbiturates. This inhibition was concentration-dependent and occurred in the range of pharmacologically effective concentrations. Pentobarbital was the most potent of the barbiturates tested with a Ki of 92 mumol/l. The (+)isomers of hexobarbital and mephobarbital were more potent than the respective (-)isomers. Barbituric acid itself did not displace either radioligand in concentrations up to 1 mmol/l. The inhibitory effect of pentobarbital was reversed by a single wash of membranes preincubated with the barbiturate. The presence of pentobarbital caused a decrease of the affinity of the receptor for the antagonist radioligand but did not alter the number of binding sites, suggesting a competitive antagonism. The effects of pentobarbital on radioligand binding to the receptor were not changed by the presence of picrotoxinin nor by the absence of chloride ions. This indicates that they are not mediated via the picrotoxinin binding site. The barbiturates could not be classified as either agonists or antagonists at the Ri adenosine receptor. The presence of GTP did not influence the inhibition of radioligand binding by pentobarbital; this is also observed for antagonists, whereas the affinity of agonists is markedly reduced by GTP. Binding of antagonists to the receptor is enthalpy-driven; the interaction of pentobarbital with the receptor was entropy-driven and the same was true for agonists.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1992

Effects of barbiturates with or without liver-tumor-promoting activity on survival and DNA synthesis of suckling and adult rat hepatocytes in serum-free primary culture.

The effects of four barbiturates with or without liver-tumor-promoting activity were examined on survival and deoxyribonucleic acid (DNA) synthesis of suckling and adult rat hepatocytes in serum-free primary culture: Of the four barbiturates, two promoters, phenobarbital and barbital, enhanced DNA synthesis of suckling rat hepatocytes at low concentrations of 0.5-2 mM or 0.5 mM, but suppressed it at high concentrations of 3 mM or 1.5-4 mM. DNA synthesis of adult rat hepatocytes was, however, only suppressed by phenobarbital within the dose range tested of 1-3 mM. On the other hand, two remaining non-promoters, barbituric acid and amobarbital, did not increase but only suppressed DNA synthesis of suckling rat hepatocytes within the dose ranges of 0.5-4 mM and 0.05-0.5 mM respectively. Phenobarbital and amobarbital were effective for supporting survival and maintaining morphological features of suckling and adult rat hepatocytes at the relatively high concentrations of 3-4 mM and 0.5-0.75 mM respectively. However, barbital and barbituric acid were ineffective for maintenance of hepatocytes. The results show that the ability to support survival of primary cultured hepatocytes is not a common property of liver-tumor-promoter barbiturates but is a common property of some barbiturates with high lipophilicity, and that the maintenance of hepatocytes by phenobarbital or amobarbital is not due to a counterbalance of stimulated proliferation and death of the cells.

Aging↗
PubMed1996

Pharmacology of barbiturate tolerance/dependence: GABAA receptors and molecular aspects.

Barbiturates are central nervous system depressants that are used as sedatives, hypnotics, anesthetics and anticonvulsants. However, prolonged use of the drugs produces physical dependence, and the drugs have a high abuse liability. The gamma-aminobutyric acidA (GABAA) receptor is one of barbiturates' main sites of action, and therefore it is thought to play a pivotal role in the development of tolerance to and dependence on barbiturates. Recent advances in the study of the GABAA receptor/chloride channel complex allow us to examine possible mechanisms that underlie barbiturate tolerance/dependence in a new light. In this minireview, we mainly focus on molecular and cellular aspects of the action of barbiturates and the possible mechanisms that contribute to development of tolerance to and dependence on barbiturates.

Animals↗
PubMed1986

Convulsant versus typical barbiturates: effects on locomotor activity.

The present studies examined the effects of a typical (secobarbital) and a convulsant (cyclohexylideneethyl-5-barbituric acid [CHEB]) barbiturate on spontaneous locomotor activity in rats. Administered alone, secobarbital produced a mild stimulation of activity at a low (2.5 mg/kg) dose, and a dose-dependent depression of locomotor activity at higher (5-20 mg/kg) doses. Surprisingly, the convulsant barbiturate CHEB produced a depression of locomotor activity at all subconvulsant doses tested (2.5-20 mg/kg). IP administration of CHEB was also observed to produce abdominal muscle contractions (writhing). In a second experiment, it was found that the writhe-inducing compound para-phenyl-quinone (PPQ) did not affect locomotor activity, indicating that the depression of activity produced by CHEB was not secondary to its writhe-producing effects. In a third experiment, the "barbiturate antagonist" potential of CHEB was examined. Treatment with 10 mg/kg CHEB did not significantly alter the depression of locomotor activity produced by 10 mg/kg secobarbital. These data suggest that (1) typical and convulsant barbiturates are not strict opposites in terms of all of their behavioral actions and (2) CHEB may not be effective as a "barbiturate antagonist."

Animals↗
PubMed1994

Dihydropyridine-sensitive calcium channels and barbiturate tolerance and withdrawal.

We have shown previously that the dihydropyridine calcium channel antagonist nitrendipine, given chronically, prevents the development of ethanol tolerance and physical dependence. The present study examines the effects on barbiturate tolerance and physical dependence. Nitrendipine, given acutely during withdrawal, provided little protection against barbiturate withdrawal, as measured by convulsive behaviour on handling. When nitrendipine was given chronically concurrently with the barbiturate, a prolonged protection against the withdrawal syndrome was seen. Acute nitrendipine significantly increased the latency of seizures in response to the partial benzodiazepine inverse agonist FG7142 during barbiturate withdrawal, but there was no effect on the seizure incidence in response to bicuculline. Chronic treatment with nitrendipine did not alter the development of tolerance to the ataxic or general anaesthetic actions of barbiturates, but evidence was found of a possible interaction between nitrendipine and pentobarbitone, which may have been pharmacokinetic. The results suggest that neuronal calcium channels may be involved to some degree in the development of the changes responsible for barbiturate withdrawal, but to a less extent than found previously for ethanol dependence.

Anesthesia, General↗