barbiturate

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(bär-bĭch'ər-ĭt, -ə-rāt', bär'bĭ-tʊr'ĭt, -āt', -tyʊr'-, bär-bĭch'ə-wĭt) pronunciation
n.
  1. A salt or ester of barbituric acid.
  2. Any of a group of barbituric acid derivatives that act as central nervous system depressants and are used as sedatives or hypnotics.

[BARBITUR(IC ACID) + -ATE2.]

USAGE NOTE   When this class of drugs was introduced in the early part of this century, barbiturate had its main stress on the penultimate syllable, a pronunciation that is still used in the medical profession. As the word passed into the general vocabulary the stress shifted to the antepenultimate syllable, bringing the stress pattern more in line with words like acculturate, accurate, and saturate. Either pronunciation is considered correct now. Since at least the 1960s the pronunciation (bär-bĭch'ə-wĭt), without the second r, has been considered nonstandard despite the fact that it is quite common. In a recent survey 62 percent of the Usage Panel still disapprove of this pronunciation, while 38 percent approve of it, suggesting that the usage is becoming less stigmatized. One reason for this may be that the pronunciation without the second r is simply easier to say, since the combination (-ər-ĭt) occurs relatively infrequently in English. In addition, the presence of the first r may influence the dropping out of the second r by the phonological process of dissimilation.



Any of a class of heterocyclic compounds based on the parent structure, uric acid, and used in medicine. They depress the central nervous system, acting particularly on certain parts of the brain, though they tend to depress the functioning of all the body's tissues. Long-acting barbiturates (e.g., barbital and phenobarbital) are used to treat epilepsy. Intermediate ones (e.g., amobarbital) are used to treat insomnia, short-acting ones (e.g., pentobarbital) to overcome difficulty in falling asleep (one aspect of insomnia), and ultra-short-acting ones (e.g., thiopental sodium) to induce unconsciousness in surgical patients before administration of other anesthetics. Prolonged use of barbiturates may lead to addiction. Sudden withdrawal can be fatal; addicts must be weaned from the drug under medical supervision. Overdoses can result in coma and even death; barbiturates are particularly dangerous, even at normal doses, when combined with alcoholic beverages.

For more information on barbiturate, visit Britannica.com.

A group of drugs widely used for the suppression of anxiety, the induction of sleep, and the control of seizures. Some of them, when injected intravenously, produce a general anesthesia. See also Anesthesia.

Barbituric acid, from which the various barbiturate congeners come, is a malonyl urea. Following the synthesis of this compound, a dozen or more closely related compounds were synthesized by adding or substituting various radicals to the general formula. The names of many of them have become familiar; examples are Phenobarbital, Meberal, Seconal, Nembutal, Amytal, and Pentothal.

These drugs act by suppressing the excitability of all tissues; but all tissues are not equally sensitive. Low dosages induce drowsiness, and high dosages coma and death. The spread between the therapeutic and fatal doses varies with the different barbiturates.

The prolonged use of these drugs results in habituation; and insomnia, agitation, confusional psychosis, and seizures may occur within 24 to 36 hours of withdrawal. Overdose is one of the commonest means of suicide in Western countries, and life can be saved only by admission to a hospital where respiration can be maintained and cerebral anoxia prevented.


Barbiturates are a group of drugs derived from barbituric acid. Barbiturates act as depressants of the central nervous system and have powerful sedative and anxiety-reducing properties. They have been commonly used in sleeping pills and to help people to relax. One of their side-effects is to interfere with the ability to perform complex skills. Barbiturates are habit-forming and prolonged use may lead to addiction.


A class of drugs that depress activity of the central nervous system; they are classified into three groups according to their duration of action: short-, intermediate-, and long-acting. Barbiturates were formerly widely used as hypnotic drugs but have largely been superseded by the benzodiazepines; they are now only prescribed for patients who are already taking them (see amobarbital; butobarbital; secobarbital). They produce tolerance and dependence; abrupt withdrawal causes severe effects similar to those seen in alcoholics deprived of alcohol. Toxic effects leading to coma and death are common after overdose, especially when accompanied by alcohol. The long-acting barbiturate phenobarbital is occasionally used in the treatment of epilepsy, and the short-acting thiopental sodium is used to induce general anaesthesia. Barbiturates are controlled drugs; they are available as tablets, capsules, or solutions for injection.

Side effects:
include 'hangover' effects with drowsiness, dizziness, shaky movements, unsteady gait, depression of breathing, headache, paradoxical excitement, and confusion. Tolerance and dependence may develop.

Precautions:
barbiturates should not be used to treat insomnia caused by uncontrolled pain; they should not be taken by women who are pregnant or breastfeeding, by people with a history of drug or alcohol abuse, or by children, young adults, or elderly people. Barbiturates should be used with caution in people who have liver or kidney disease.

Interactions with other drugs:

Anticoagulants the anticoagulant effects of warfarin and acenocoumarol are reduced by barbiturates.
Antiviral drugs the plasma concentrations of indinavir, nelfinavir, and saquinavir may be reduced by barbiturates; phenobarbital may reduce the plasma concentrations of other antivirals, including Kaletra.
Calcium antagonists the effects of diltiazem, felodipine, isradipine, verapamil, and probably nicardipine and nifedipine are reduced by barbiturates.
Ciclosporin: its effects are reduced by barbiturates.
Corticosteroids their effects are reduced by barbiturates.
Oral contraceptives their effects are reduced by barbiturates.
Sodium oxybate its effects are enhanced by barbiturates and it should not be used with these drugs.

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Drugs derived from barbituric acid. Barbiturates are depressants of the central nervous system, and have powerful anxiolytic and sedative properties. They have been commonly used in sleeping pills. Their effects are likely to disrupt the performance of complex motor skills. Habitual use of barbiturates can result in a true addiction.

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barbiturate (bärbĭch'ərāt'), any one of a group of drugs that act as depressants on the central nervous system. High doses depress both nerve and muscle activity and inhibit oxygen consumption in the tissues. In low doses barbiturates act as sedatives, i.e., they have a tranquilizing effect; increased doses have a hypnotic or sleep-inducing effect; still larger doses have anticonvulsant and anesthetic activity. The mechanism of action on the central nervous system is not known. The barbiturates are all derivatives of barbituric acid, which was first prepared in 1864 by the German organic chemist Adolf von Baeyer.

The drugs differ widely in the duration of their action, which depends on the rapidity with which they are distributed in body tissues, degraded, and excreted. Ultrashort-acting barbiturates such as thiopental sodium (Pentothal) are often used as general anesthetics. Secobarbital (Seconal) and pentobarbital sodium (Nembutal) are short-acting barbiturates, amobarbital (Amytal) is intermediate in duration of action, and phenobarbital (Luminal) is a long-acting derivative.

Barbiturates are used to relax patients before surgery, as anticonvulsants, and as sleeping pills. They also are commonly abused. Taken regularly, barbiturates can be psychologically and physically addictive (see drug addiction and drug abuse). Barbiturate addicts must be withdrawn from the drug gradually to avoid severe withdrawal symptoms such as convulsions. Overdose can cause coma or death. In the United States the manufacture and distribution of barbiturates were brought under federal control by the 1965 Drug Abuse and Control Act, and they are legally available only by prescription.

Bibliography

See publications of the Drugs & Crime Data Center and Clearinghouse, the Bureau of Justice Statistics Clearinghouse, and the National Clearinghouse for Alcohol and Drug Information.


(bahr-bich-uh-rits, bahr-bich-uh-rayts)

Substances derived from an organic compound that are used as sedatives and sleep inducers. Barbiturates, which work by depressing the activity of the central nervous system, are sometimes used in the treatment of illnesses such as epilepsy.

  1. the tautomeric anion derived from barbituric acid (malonylurea; 2,4,6(1H,3H,5H)-pyrimidinetrione).
  2. any mixture of free barbituric acid and its anion.
  3. any salt of barbituric acid.
  4. any of various pharmacologically active derivatives of barbituric acid, including barbitone, pentobarbitone, phenobarbitone, and thiopentone. Barbiturates are potent CNS depressants that potentiate the actions of GABA by binding to the GABAA receptor. Pentobarbitone and thiopentone are used to induce anesthesia.

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Any of a group of organic compounds derived from barbituric acid. There are a number of barbiturates. They all depress the nervous system and are used to induce apathy and sleep, and in high doses, as anesthetics. They vary in their sedative effects, in the duration of their effectiveness and in their toxicity. Those that are used in veterinary medicine are: (1) pentobarbital sodium (Nembutal); largely superseded, but still sometimes used for intravenous anesthesia in companion animals; (2) thiopental sodium, which has a short period of effectiveness, an advantage in many veterinary situations, e.g. examination of a pharynx; (3) thialbarbital sodium, a medium length compound; (4) thiamylal sodium, a compound with ultrashort action.

  • b. slough — skin slough over a vein where a solution of barbiturate intended for injection into the vein leaks into subcutaneous tissue.
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(bär-bich′ǒǒr-āt)
n

A derivative of barbituric acid that acts as a sedative or hypnotic. Barbiturates are controlled substances that have addictive potentials.

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categories related to 'barbiturate'

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Random House Word Menu by Stephen Glazier
For a list of words related to barbiturate, see:
  • PHARMACOLOGY - barbiturate: barbituric acid derivative that depresses central nervous system activity, induces sleep, and produces tolerance
  • Drug Names and Forms - barbiturate: pharmaceutical central nervous system depressant and muscle relaxer


  See crossword solutions for the clue Barbiturate.
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Barbituric acid, the basic structure of all barbiturates

Barbiturates are drugs that act as central nervous system depressants, and can therefore produce a wide spectrum of effects, from mild sedation to total anesthesia. They are also effective as anxiolytics, as hypnotics, and as anticonvulsants. Barbiturates also have analgesic effects, however these effects are somewhat weak, preventing barbiturates from being used in surgery in the absence of other analgesics. They have addiction potential, both physical and psychological. Barbiturates have now largely been replaced by benzodiazepines in routine medical practice - for example, in the treatment of anxiety and insomnia – mainly because benzodiazepines are significantly less dangerous in overdose. However, barbiturates are still used in general anesthesia, for epilepsy, and assisted suicide.[1] Barbiturates are derivatives of barbituric acid.[2]

Contents

History

Barbituric acid was first synthesized December 6, 1864, by German researcher Adolf von Baeyer. This was done by condensing urea (an animal waste product) with diethyl malonate (an ester derived from the acid of apples). There are several stories about how the substance got its name. The most likely story is that Von Baeyer and his colleagues went to celebrate their discovery in a tavern where the town's artillery garrison were also celebrating the feast of Saint Barbara—the patron saint of artillerists. An artillery officer is said to have christened the new substance by amalgamating Barbara with urea.[3] Another story holds that Von Baeyer synthesized the substance from the collected urine of a Munich waitress named Barbara.[4] No substance of medical value was discovered, however, until 1903 when two German scientists working at Bayer, Emil Fischer and Joseph von Mering, discovered that barbital was very effective in putting dogs to sleep. Barbital was then marketed by Bayer under the trade name Veronal. It is said that Von Mering proposed this name because the most peaceful place he knew was the Italian city of Verona.[3]

It was not until the 1950s that the behavioural disturbances and physical dependence potential of barbiturates became recognized.[5]

While barbituric acid itself does not have any direct effect on the central nervous system, chemists have derived over 2,500 compounds from it that possess pharmacologically active qualities. The broad class of barbiturates is further broken down and classified according to speed of onset and duration of action. Ultrashort-acting barbiturates are commonly used for anesthesia because their extremely short duration of action allows for greater control. These properties allow doctors to rapidly put a patient "under" in emergency surgery situations. Doctors can also bring a patient out of anesthesia just as quickly, should complications arise during surgery. The middle two classes of barbiturates are often combined under the title "short/intermediate-acting." These barbiturates are also employed for anesthetic purposes, and are also sometimes prescribed for anxiety or insomnia. This is not a common practice anymore, however, owing to the dangers of long-term use of barbiturates; they have been replaced by the benzodiazepines for these purposes. The final class of barbiturates are known as long-acting barbiturates (the most notable one being phenobarbital, which has a half-life of roughly 92 hours). This class of barbiturates is used almost exclusively as anticonvulsants, although on rare occasions they are prescribed for daytime sedation. Barbiturates in this class are not used for insomnia, because, owing to their extremely long half-life, patients would awake with a residual "hang-over" effect and feel groggy.

Barbiturates can in most cases be used either as the free acid or as salts of sodium, calcium, potassium, magnesium, lithium, etc. Codeine- and Dionine-based salts of barbituric acid have been developed. In 1912, Bayer introduced another barbituric acid derivative, phenobarbital, under the trade name Luminal, as a sedative-hypnotic.[6]

Therapeutic uses

Barbiturates such as phenobarbital were long used as anxiolytics and hypnotics. Today, benzodiazepines have largely supplanted them for these purposes, because benzodiazepines have less potential for lethal overdoses.[7][8][9]

Other uses related to their physiological properties

Barbiturates in high doses are used for physician-assisted suicide (PAS), and in combination with a muscle relaxant for euthanasia and for capital punishment by lethal injection.[10][11] Thiopental is an ultra-short acting barbiturate that is marketed under the name sodium pentothal. It is often mistaken for "truth serum" or sodium amytal, an intermediate-acting barbiturate that is used for sedation and to treat insomnia, but was also used in so-called sodium amytal "interviews" where the person being questioned would be much more likely to provide the truth whilst under the influence of this drug. When dissolved in water, sodium amytal can be swallowed, or it can be administered by intravenous injection. The drug does not itself force people to tell the truth, but is thought to decrease inhibitions, making subjects more likely to be caught off guard when questioned.[12]

Mechanism of action

The principal mechanism of action of barbiturates is believed to be their affinity for the GABAA receptor (Acts on GABA : BDZ receptor Cl- channel complex). GABA is the principal inhibitory neurotransmitter in the mammalian central nervous system (CNS). Barbiturates bind to the GABAA receptor at the beta subunit, which are binding sites distinct from GABA itself and also distinct from the benzodiazepine binding site. Like benzodiazepines, barbiturates potentiate the effect of GABA at this receptor. In addition to this GABA-ergic effect, barbiturates also block the AMPA receptor, a subtype of glutamate receptor. Glutamate is the principal excitatory neurotransmitter in the mammalian CNS. Taken together, the findings that barbiturates potentiate inhibitory GABAA receptors and inhibit excitatory AMPA receptors can explain the CNS-depressant effects of these agents. At higher concentration, they inhibit the Ca2+-dependent release of neurotransmitters.[13] Barbiturates produce their pharmacological effects by increasing the duration of chloride ion channel opening at the GABAA receptor (pharmacodynamics: This increases the efficacy of GABA), whereas benzodiazepines increase the frequency of the chloride ion channel opening at the GABAA receptor (pharmacodynamics: This increases the potency of GABA). The direct gating or opening of the chloride ion channel is the reason for the increased toxicity of barbiturates compared to benzodiazepines in overdose.[14][15]

Further, barbiturates are relatively non-selective compounds that bind to an entire superfamily of ligand-gated ion channels, of which the GABAA receptor channel is only one of several representatives. This superfamily of ion channels includes the neuronal nAChR channel, the 5HT3R channel, the GlyR channel and others. However, while GABAA receptor currents are increased by barbiturates (and other general anaesthetics), ligand-gated ion channels that are predominantly permeable for cationic ions are blocked by these compounds. For example, neuronal nAChR channels are blocked by clinically relevant anaesthetic concentrations of both thiopental and pentobarbital.[16] Such findings implicate (non-GABA-ergic) ligand-gated ion channels, e.g. the neuronal nAChR channel, in mediating some of the (side) effects of barbiturates.[17]

Tolerance, dependence, overdose, and adverse reaction

Older adults and pregnant women and babies should consider the risks associated with barbiturate use. When a person ages, the body becomes less able to rid itself of barbiturates. As a result, people over the age of sixty-five are at higher risk of experiencing the harmful effects of barbiturates, including drug dependence and accidental overdose.[18] When barbiturates are taken during pregnancy, the drug passes through the mother's bloodstream to her fetus. After the baby is born, it may experience withdrawal symptoms and have trouble breathing. In addition, nursing mothers who take barbiturates may transmit the drug to their babies through breast milk.[19]

Tolerance and dependence

With regular use, tolerance to the effects of barbiturates develops.

Overdose

Symptoms of an overdose typically include sluggishness, incoordination, difficulty in thinking, slowness of speech, faulty judgment, drowsiness, shallow breathing, staggering, and in severe cases coma and death. The lethal dosage of barbiturates varies greatly with tolerance and from one individual to another. The amount of 1 g in dose orally can be highly poisonous with dosages from 2g to 10 g being generally fatal depending on the person tolerance level. Even in inpatient settings, however, the development of tolerance is still a problem, as dangerous and unpleasant withdrawal symptoms can result when the drug is stopped after dependence has developed. Barbiturates in overdose with other CNS (central nervous system) depressants for example, alcohol, opiates or benzodiazepines is even more dangerous due to additive CNS and respiratory depressant effects. In the case of benzodiazepines not only do they have additive effects, barbiturates also increase the binding affinity of the benzodiazepine binding site thus leading to an exaggerated effect of benzodiazepines.

Marilyn Monroe and Judy Garland both died of barbiturate overdose.

Adverse reaction

A rare adverse reaction to barbiturates is Stevens–Johnson syndrome, which primarily affects the mucous membranes.

Recreational use

Barbiturates produce effects similar to ethanol during intoxication. The symptoms of barbiturate intoxication include respiratory depression, lowered blood pressure, fatigue, fever, unusual excitement, irritability, dizziness, poor concentration, sedation, confusion, impaired coordination, impaired judgment, addiction, and respiratory arrest, which may lead to death.[20]

Recreational users[who?] report that a barbiturate high gives them feelings of relaxed contentment and euphoria. The main risk of acute barbiturate abuse is respiratory depression. Physical and psychological dependence may also develop with repeated use.[21] Other effects of barbiturate intoxication include drowsiness, lateral and vertical nystagmus, slurred speech and ataxia, decreased anxiety, a loss of inhibitions. Barbiturates are also used to alleviate the adverse or withdrawal effects of illicit drug misuse.[22][23]

Drug users tend to prefer short-acting and intermediate-acting barbiturates.[24] The most commonly abused are amobarbital (Amytal), pentobarbital (Nembutal), and secobarbital (Seconal). A combination of amobarbital and secobarbital (called Tuinal) is also highly abused. Short-acting and intermediate-acting barbiturates are usually prescribed as sedatives and sleeping pills. These pills begin acting fifteen to forty minutes after they are swallowed, and their effects last from five to six hours. Veterinarians use pentobarbital to anesthetise animals before surgery; in large doses, it can be used to euthanise animals.[25]

Slang terms for barbiturates include barbs, bluebirds, dolls, downers, goofballs, sleepers and tooties.[26]

Legal status

In the 1940s, military personnel were given "Goofballs" during WWII in the South Pacific region to allow soldiers to tolerate the heat and humidity of daily working conditions. Goofballs were distributed to lower the respiratory system and blood pressure to combat the extreme conditions. Many soldiers returned with addictions that required several months of rehabilitation before discharge. This led to addiction problems through the 1950s and 1960s.

In the 1950s and 1960s, increasing reports began to be published about barbiturate overdoses and dependence problems, which eventually led to the scheduling of barbiturates as controlled drugs.

In 1970, several barbiturates were designated in the United States as controlled substances with the passage of the American Controlled Substances Act of 1970. Pentobarbital, secobarbital and amobarbital were designated schedule II drugs, butabarbital schedule III, and barbital and phenobarbital schedule IV.

In 1971, the Convention on Psychotropic Substances was signed in Vienna. Designed to regulate amphetamines, barbiturates, and other synthetics, the treaty today regulates secobarbital, amobarbital, butalbital, cyclobarbital, and pentobarbital as schedule III, and allobarbital, methylphenobarbital, phenobarbital, and vinylbital as schedule IV scheduled substances.

Other uses in chemistry

In 1988, the synthesis and binding studies of an artificial receptor binding barbiturates by 6 complementary hydrogen bonds was published.[27] Since this first article, different kind of receptors were designed, as well as different barbiturates and cyanurates, not for their efficiencies as drugs but for applications in supramolecular chemistry, in the conception of materials and molecular devices.

Examples

generic structure of a barbiturate, including numbering scheme
Barbiturates
Short Name R1 R2 IUPAC Name
Allobarbital CH2CHCH2 CH2CHCH2 5,5-diallylbarbiturate
Amobarbital CH2CH3 CH2CH2CH(CH3)2 5-ethyl-5-isopentyl-barbiturate
Aprobarbital CH2CHCH2 CH(CH3)2 5-allyl-5-isopropyl-barbiturate
Alphenal CH2CHCH2 C6H5 5-allyl-5-phenyl-barbiturate
Barbital CH2CH3 CH2CH3 5,5-diethylbarbiturate
Brallobarbital CH2CHCH2 CH2CBrCH2 5-allyl-5-(2-bromo-allyl)-barbiturate
Phenobarbital CH2CH3 C6H5 5-ethyl-5-phenylbarbiturate

See also

References

  1. ^ "DIGNITAS". http://www.dignitas.ch/index.php?option=com_content&view=article&id=22&Itemid=62&lang=de. Retrieved 2011-06-14. 
  2. ^ Kinetics of hydrolysis of barbituric acid derivatives. 21 SEP 2006. doi:10.1002/jps.2600600807. http://onlinelibrary.wiley.com/doi/10.1002/jps.2600600807/abstract. 
  3. ^ a b "Barbiturates". http://www.ch.ic.ac.uk/rzepa/mim/drugs/html/barbiturate_text.htm. Retrieved 2007-10-31. 
  4. ^ Medical Curiosities. Youngson, Robert M. London: Robinson Publishing, 1997. Page 276.
  5. ^ Galanter, Marc; Kleber, Herbert D. (1 July 2008). The American Psychiatric Publishing Textbook of Substance Abuse Treatment (4th ed.). United States of America: American Psychiatric Publishing Inc. p. 217. ISBN 978-1-58562-276-4. http://books.google.com/?id=6wdJgejlQzYC. 
  6. ^ Sneader, Walter (2005-06-23). Drug Discovery. John Wiley and Sons. pp. 369. ISBN 0-471-89979-8. 
  7. ^ Whitlock FA (June 14, 1975). "Suicide in Brisbane, 1956 to 1973: the drug-death epidemic". Med J Aust 1 (24): 737–43. PMID 239307. 
  8. ^ Johns MW (1975). "Sleepy and hypnotic drugs". Drugs 9 (6): 448–78. doi:10.2165/00003495-197509060-00004. PMID 238826. 
  9. ^ Jufe GS (Jul-August 2007). "[New hypnotics: perspectives from sleep physiology]". Vertex 18 (74): 294–9. PMID 18265473. 
  10. ^ "Administration and Compounding Of Euthanasic Agents". http://www.wweek.com/___ALL_OLD_HTML/euthanasics.html. Retrieved 15 July 2008. 
  11. ^ Daniel Engber. "Why do lethal injections have three drugs?". Slate Magazine. http://www.slate.com/id/2141000/. Retrieved 15 July 2008. 
  12. ^ "Neuroscience for Kids - Barbiturates". http://faculty.washington.edu/chudler/barb.html. Retrieved 2008-06-02. 
  13. ^ Brunton, Laurence L.; Lazo, John S.; Parker, Keith L.; Goodman, Louis Sanford; Gilman, Alfred Goodman (2005). Goodman & Gilman's Pharmacological Basis of Therapeutics. McGraw-Hill. ISBN 0-07-142280-3. 
  14. ^ Neil Harrison; Wallace B Mendelson and Harriet de Wit (2000). "Barbiturates". Neuropsychopharmacology. http://www.acnp.org/g4/GN401000173/CH169.html. Retrieved 15 July 2008. 
  15. ^ Society for Neurochemistry, American; George J. Siegel M.D., Bernard W. Agranoff M.D., Stephen K. Fisher Ph.D., R. Wayne Albers Ph.D., Michael D. Uhler Ph.D. (1999) [1998]. "Part 2 Chapter 16". Basic Neurochemistry - Molecular, Cellular and Medical Aspects (Sixth ed.). Lippincott Williams and Wilkins. ISBN 0-397-51820-X. http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=bnchm.section.1181. Retrieved July 2008. 
  16. ^ Weber, M; Motin, L; Gaul, S; Beker, F; Fink, RH; Adams, DJ (January 2005). "Intravenous anaesthetics inhibit nicotinic acetylcholine receptor-mediated currents and Ca2+ transients in rat intracardiac ganglion neurons". British Journal of Pharmacology 144 (1): 98–107. doi:10.1038/sj.bjp.0705942. PMC 1575970. PMID 15644873. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1575970. 
  17. ^ Franks, NP; Lieb, WR (23 November 1998). "Which molecular targets are most relevant to general anaesthesia?". Toxicology Letters 100–101: 1–8. doi:10.1016/S0378-4274(98)00158-1. PMID 10049127. 
  18. ^ WebMD. "Toxicity, Barbiturate". eMedicine. http://www.emedicine.com/MED/topic207.htm. Retrieved 15 July 2008. 
  19. ^ Nau H; Kuhnz W, Egger HJ, Rating D, Helge H (Nov-December 1982). "Anticonvulsants during pregnancy and lactation. Transplacental, maternal and neonatal pharmacokinetics". Clin Pharmacokinet 7 (6): 508–43. doi:10.2165/00003088-198207060-00003. PMID 6819105. 
  20. ^ National Institute on Drug Abuse. "Commonly Abused Drugs". pp. 1. http://www.drugabuse.gov/DrugPages/DrugsofAbuse.html. Retrieved 15 July 2008. 
  21. ^ Schlatter J; Sitbon N, Saulnier JL (February 17, 2001). "[Drugs and drug abusers]". Presse Med 30 (6): 282–7. PMID 11252979. 
  22. ^ Emedicine Health. "Barbiturate Abuse". pp. 1. http://www.emedicinehealth.com/barbiturate_abuse/article_em.htm. Retrieved 15 July 2008. 
  23. ^ Faulkner TP; Hayden JH, Mehta CM, Olson DA, Comstock EG (1979). "Dose-response studies on tolerance to multiple doses of secobarbital and methaqualone in a polydrug abuse population". Clin Toxicol 15 (1): 23–37. doi:10.3109/15563657908992476. PMID 498734. 
  24. ^ Coupey SM (August 1997). "Barbiturates". Pediatr Rev 18 (8): 260–4. doi:10.1542/pir.18-8-260. PMID 9255991. 
  25. ^ DEA Brief on Barbiturates
  26. ^ Hamid H.; El-Mallakh RS, Vandeveir K (March 2005). "Substance Abuse: Medical and Slang Terminology". South Med J (Medscape) 98 (3): 350–362. doi:10.1097/01.SMJ.0000153639.23135.6A. PMID 15813163. http://www.medscape.com/viewarticle/501975_4. 
  27. ^ Chang, Suk Kyu.; Hamilton, Andrew D. (1988). "Molecular recognition of biologically interesting substrates: Synthesis of an artificial receptor for barbiturates employing six hydrogen bonds". Journal of the American Chemical Society 110 (4): 1318–1319. doi:10.1021/ja00212a065. 

External links



Translations:

Barbiturate

Top

Dansk (Danish)
n. - barbiturat

Nederlands (Dutch)
slaappil, barbituraat

Français (French)
n. - barbiturique

Deutsch (German)
n. - Schlaftablette, Barbiturat

Ελληνική (Greek)
n. - βαρβιτουρικό

Italiano (Italian)
barbiturico

Português (Portuguese)
n. - barbiturato (m) (Quím.)

Русский (Russian)
барбитурат

Español (Spanish)
n. - barbitúrico

Svenska (Swedish)
n. - barbiturat, sömntablett

中文(简体)(Chinese (Simplified))
巴比妥酸盐

中文(繁體)(Chinese (Traditional))
n. - 巴比妥酸鹽

한국어 (Korean)
n. - 바르비투르산염 유도제[진정제, 수면제]

日本語 (Japanese)
n. - バルビツール酸塩, バルビツール剤

العربيه (Arabic)
‏(الاسم) نوع من المخدرات‏

עברית (Hebrew)
n. - ‮תרופת הרגעה‬


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