Bemegride
Electronic Mail
Messages between computer users via COMPUTER COMMUNICATION NETWORKS. This feature duplicates most of the features of paper mail, such as forwarding, multiple copies, and attachments of images and other file types, but with a speed advantage. The term also refers to an individual message sent in this way.
Editorial Policies
Authorship
Postal Service
Internet
Doxapram
Barbiturates
Coproporphyria, Hereditary
An autosomal dominant porphyria that is due to a deficiency of COPROPORPHYRINOGEN OXIDASE in the LIVER, the sixth enzyme in the 8-enzyme biosynthetic pathway of HEME. Clinical features include both neurological symptoms and cutaneous lesions. Patients excrete increased levels of porphyrin precursors, 5-AMINOLEVULINATE and COPROPORPHYRINS.
Coproporphyrins
Coproporphyrinogen Oxidase
An enzyme that catalyzes the oxidative decarboxylation of coproporphyrinogen III to protoporphyrinogen IX by the conversion of two propionate groups to two vinyl groups. It is the sixth enzyme in the 8-enzyme biosynthetic pathway of HEME, and is encoded by CPO gene. Mutations of CPO gene result in HEREDITARY COPROPORPHYRIA.
Porphyrias, Hepatic
A group of metabolic diseases due to deficiency of one of a number of LIVER enzymes in the biosynthetic pathway of HEME. They are characterized by the accumulation and increased excretion of PORPHYRINS or its precursors. Clinical features include neurological symptoms (PORPHYRIA, ACUTE INTERMITTENT), cutaneous lesions due to photosensitivity (PORPHYRIA CUTANEA TARDA), or both (HEREDITARY COPROPORPHYRIA). Hepatic porphyrias can be hereditary or acquired as a result of toxicity to the hepatic tissues.
Porphyrias
A diverse group of metabolic diseases characterized by errors in the biosynthetic pathway of HEME in the LIVER, the BONE MARROW, or both. They are classified by the deficiency of specific enzymes, the tissue site of enzyme defect, or the clinical features that include neurological (acute) or cutaneous (skin lesions). Porphyrias can be hereditary or acquired as a result of toxicity to the hepatic or erythropoietic marrow tissues.
Porphyrins
A group of compounds containing the porphin structure, four pyrrole rings connected by methine bridges in a cyclic configuration to which a variety of side chains are attached. The nature of the side chain is indicated by a prefix, as uroporphyrin, hematoporphyrin, etc. The porphyrins, in combination with iron, form the heme component in biologically significant compounds such as hemoglobin and myoglobin.
Porphyrinogens
Organophosphonates
Amination
Molecular Structure
Phosphorus
Structure-Activity Relationship
Stereoisomerism
Double-Blind Method
Clinical Trials as Topic
Works about pre-planned studies of the safety, efficacy, or optimum dosage schedule (if appropriate) of one or more diagnostic, therapeutic, or prophylactic drugs, devices, or techniques selected according to predetermined criteria of eligibility and observed for predefined evidence of favorable and unfavorable effects. This concept includes clinical trials conducted both in the U.S. and in other countries.
Surgical Procedures, Minor
Cross-Over Studies
Studies comparing two or more treatments or interventions in which the subjects or patients, upon completion of the course of one treatment, are switched to another. In the case of two treatments, A and B, half the subjects are randomly allocated to receive these in the order A, B and half to receive them in the order B, A. A criticism of this design is that effects of the first treatment may carry over into the period when the second is given. (Last, A Dictionary of Epidemiology, 2d ed)
Color
Tranquilizing Agents
A traditional grouping of drugs said to have a soothing or calming effect on mood, thought, or behavior. Included here are the ANTI-ANXIETY AGENTS (minor tranquilizers), ANTIMANIC AGENTS, and the ANTIPSYCHOTIC AGENTS (major tranquilizers). These drugs act by different mechanisms and are used for different therapeutic purposes.
Chemistry, Pharmaceutical
Encyclopedias as Topic
Opiate Alkaloids
Hypnotics and Sedatives
Receptors, GABA-A
Search Engine
Genome, Human
Receptors, GABA
Cell-surface proteins that bind GAMMA-AMINOBUTYRIC ACID with high affinity and trigger changes that influence the behavior of cells. GABA-A receptors control chloride channels formed by the receptor complex itself. They are blocked by bicuculline and usually have modulatory sites sensitive to benzodiazepines and barbiturates. GABA-B receptors act through G-proteins on several effector systems, are insensitive to bicuculline, and have a high affinity for L-baclofen.
Antibodies
Genetic Code
Drug Users
Work Capacity Evaluation
Primidone
Anemia, Megaloblastic
Chemical Industry
Epilepsy
A disorder characterized by recurrent episodes of paroxysmal brain dysfunction due to a sudden, disorderly, and excessive neuronal discharge. Epilepsy classification systems are generally based upon: (1) clinical features of the seizure episodes (e.g., motor seizure), (2) etiology (e.g., post-traumatic), (3) anatomic site of seizure origin (e.g., frontal lobe seizure), (4) tendency to spread to other structures in the brain, and (5) temporal patterns (e.g., nocturnal epilepsy). (From Adams et al., Principles of Neurology, 6th ed, p313)
Actions of steroids and bemegride on the GABAA receptor of mouse spinal neurones in culture. (1/14)
The effects of a synthetic and an endogenous steroid were studied on the GABAA receptors of isolated mouse spinal neurones, maintained in culture. Low doses of alphaxalone reversibly increased GABA-evoked whole-cell currents. Alphaxalone at higher doses (10-50 microM), when pressure ejected onto spinal neurones, also directly evoked a membrane chloride current. Such currents were reversibly suppressed by bicuculline (a GABAA antagonist) and enhanced by phenobarbitone. 5 beta-Pregnan-3 alpha-ol-20-one, a progesterone metabolite, dose-dependently potentiated the amplitude of GABA-evoked whole-cell currents. The mechanism of potentiation was examined at the single-channel level using outside-out patches from spinal neurones. The main action of the steroid on the GABAA receptor appears to be similar to that found for barbiturates, in that they prolonged GABA-activated bursts of channel openings. Bemegride had an antagonistic action on the GABAA receptor, suppressing both GABA- and pentobarbitone-evoked whole-cell currents to similar extents. (+info)Carisoprodol tolerance and precipitated withdrawal. (2/14)
(+info)An analysis of the drugs acting on cerebral energy metabolism. (3/14)
The behaviour of (a) the redox potential of the lactate/pyruvate system and the changes of the redox potential of the lactate/pyruvate system across the brain; (b) the energy charge potential of the adenylate pool, was studied in the brain of curarized beagle dogs. The influence of certain drugs (amobarbital, nicergoline, theophylline, papaverine, bamethan, dipyridamole, bemegride) on these parameters was evaluated under control conditions, during hypoxemia and during post-hypoxiemic recovery. On the whole, the action on energetic metabolism appears to be unrelated to the action believed to be exerted by drugs on cerebral vessels. (+info)Effects of drugs acting alone and in combination on the motor activity of intact mice. (4/14)
1. When administered to intact white mice, the central depressants-diphenhydramine, promethazine, chlorpromazine, gammahydroxybutyrate, gammabutyrolactone, hyoscine, and pethidine-produced sedation in small doses, but excitement and convulsions in higher doses. When given to mice pretreated with subanaesthetic doses of phenobarbitone these drugs abolished the righting reflex both in convulsant doses (hyoscine excepted) and in non-convulsant doses. These effects are similar to the effects previously observed with local anaesthetics.2. Meprobamate, diazepam and chlorpromazine produced a loss of righting reflex both when given alone and following phenobarbitone. When given alone in higher doses, chlorpromazine induced convulsions.3. The central stimulants bemegride and picrotoxin antagonized the loss of righting reflex produced by phenobarbitone, but nikethamide, caffeine and strychnine did not alter the depressant effects of phenobarbitone.4. On the basis of these and previous studies with intact white mice a tentative classification of drugs having generalized depressant and stimulant effects on the central nervous system was proposed and discussed. (+info)Effects of general stimulant drugs on the electrical responses of isolated slabs of cat's cerebral cortex. (5/14)
1. In the neuronally isolated cortex of the cat, local application of bemegride, picrotoxin, nikethamide, caffeine and strychnine facilitated the surface positive response of the isolated cortex and lowered the stimulus threshold for this response. Excepting nikethamide, they all produced convulsive discharge in the isolated cortex unrelated to the applied stimulus.2. Local application of glutamate to the cortex produced spreading depression, which was sometimes preceded by spontaneous positive bursting.3. In contrast to the "general depressants" which produce a relatively consistent pattern of effects on the electrical responses of isolated cortex, the "general stimulants", although they all have excitatory effects on isolated cortex, each produced a greatly different type of electrical response in the isolated cortex, suggesting that several different mechanisms of action are responsible for their effects. (+info)Physiological and drug-induced changes in the glycogen content of mouse brain. (6/14)
1. The effect of the method of killing on the concentration of glycogen in mouse brain was determined. The cerebral glycogen content of mice killed by immersion in liquid nitrogen did not differe significantly from that of animals decapitated and the heads immediately frozen. A delay before freezing led to the rapid loss of brain glycogen, with a 17% fall at 10 s and an 82% loss after 5 min.2. Hyperglycaemia, induced by the administration of D-glucose, resulted in an 8.3% loss of brain glycogen after 120 min. Insulin hypoglycaemia produced a 10.7% fall in glycogen at 60 min followed by an 11.2% increase at 120 min.3. Exposure to either high (32 degrees C) or low (10 degrees C) ambient temperatures caused a depletion of brain glycogen.4. A circadian rhythm of brain glycogen concentration was found, with a nadir which was coincident with the peak of locomotor activity and body temperature.5. Drugs from several pharmacological classes were studied for their in vivo effect on the concentration of glycogen in mouse brain.6. Brain glycogen was increased by all the depressant drugs tested, and by some drugs which had little effect on behaviour (diphenhydramine, phenytoin and propranolol), or which caused excitation (caffeine and nialamide).7. Glycogen was depleted only by amphetamine-like compounds or by bemegride-induced convulsions.8. The results are discussed with particular reference to the possible relation between catecholamines and glycogen metabolism in the brain. (+info)Postsynaptic effects of some central stimulants at the neuromuscular junction. (7/14)
1 Miniature endplate currents (m.e.p.cs) were recorded with extracellular electrodes from sartorius muscles of toads. 2 Central excitant analogues of amylobarbitone (3M2B) and halothane (DBE) decreased the amplitude and time constant of decay of m.e.p.cs and hence reduced the amplitude of miniature endplate potentials. The decay remained exponential with single time constant. 3 A central excitant analogue of ether (indoklon) reduced the amplitude of m.e.p.cs and made their decay biphasic. The decay could be fitted by the sum of two exponentials. 4 Bemegride, a central excitant, prolonged m.e.p.cs. Their decay remained exponential with single time constant. The effect was not due to inhibition of acetylcholinesterase. 5 All of the drugs tested, including amylobarbitone, reduced the temperature-sensitivity of the decay of m.e.p.cs. 6 The biphasic decay of m.e.p.cs caused by indoklon could not be explained simply by supposing that the drug blocked open endplate channels unless it was assumed that the normal rate of channel closing also increased and became much less temperature-sensitive than normal. (+info)Studies on the muscle relaxation effects of ethyl loflazepate (CM6912) and evaluation as an anti-anxiety drug. (8/14)
A new anti-anxiety drug, CM6912 (ethyl loflazepate, ethyl 7-chloro-2,3-dihydro-5-(2-fluorophenyl)-2-oxo-1H-1,4-benzodiazepine-3- carboxylate), was investigated for its effects on the alpha- and gamma-motor systems and on the cooperative muscular motions and for its interactions with other CNS drugs. The results obtained are as follows: Muscular discharges (EMG) induced by decerebrate rigidity were unaffected by 10 mg/kg (p.o.) of CM6912, but the amplitudes of the EMG were reduced by 50% for 3 hr by 30 mg/kg of CM6912 at 30 min after administration. Diazepam (10 mg/kg) also decreased the amplitudes of the EMG even at 5 min after administration, indicating that diazepam had a stronger than CM6912. Both monosynaptic spinal reflex (MSR) and polysynaptic spinal reflex (PSR) were unaffected by CM6912 (100 mg/kg). Dorsal root reflex potential was slightly enhanced by CM6912 (100 mg/kg), but not at a dose of 30 mg/kg. Diazepam (10 mg/kg) did not decrease MSR, but slightly reduced PSR. Dorsal root reflex potential was almost doubled by diazepam. The frequency of spontaneous discharges of Gla spindle afferent fiber of the extensor muscle of the hindlimb of anesthetized cats was unchanged by 10 mg/kg CM6912, but was suppressed by diazepam at the same dose while at a dose of 30 mg/kg, it was reduced mildly by CM6912, and markedly by diazepam. ED50 values for the antagonistic action on bemegride-induced convulsions were 0.30 mg/kg for CM6912 and 0.49 mg/kg for diazepam at 1 hr after administration, and they were 0.30 mg/kg and 0.67 mg/kg for CM6912 and diazepam, respectively, at 4 hr. The potentiating action of CM6912 on chlorprothixene-induced anesthesia was far weaker than that of diazepam. The suppressive potency of CM6912 on the adaptability to the rotarod was about half that of diazepam, and the muscle relaxant action of CM6912, examined by the inclined board test and the hanging test, was found to be similar to that of diazepam. These results suggest that CM6912 is less potent than diazepam in reducing muscular tone and in inducing sleep, while it has a stronger and longer-lasting anti-anxietic activity than diazepam. (+info)
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Amiphenazole
Mears GW (March 1958). "Massive doses of bemegride and amiphenazole in treatment of barbiturate poisoning". British Medical ... Dotevall G, Herner B (August 1957). "Treatment of acute primidone poisoning with bemegride and amiphenazole". British Medical ... Worlock A (November 1956). "Barbiturate poisoning treated with amiphenazole and bemegride". British Medical Journal. 2 (5001): ... Rowell NR (February 1957). "Treatment of glutethimide poisoning with bemegride and amiphenazole". Lancet. 272 (6965): 407-9. ...
Primidone
Treatments for primidone overdose have included hemoperfusion with forced diuresis, a combination of bemegride and amiphenazole ... Dotevall, Gerhard; Birger Herner (August 24, 1957). "Treatment of Acute Primidone Poisoning with Bemegride and Amiphenazole". ... and a combination of bemegride, spironolactone, caffeine, pentylenetetrazol, strophanthin, penicillin and streptomycin. In the ...
Primidone
Treatments for primidone overdose have included hemoperfusion with forced diuresis,[48] a combination of bemegride and ... "Treatment of Acute Primidone Poisoning with Bemegride and Amiphenazole". British Medical Journal. 2 (5042): 451-2. doi:10.1136 ... amiphenazole;[51] and a combination of bemegride, spironolactone, caffeine, pentylenetetrazol, strophanthin, penicillin and ...
Convulsant
Bemegride and flumazenil are used to treat drug overdoses (of barbiturates and benzodiazepines respectively), but may cause ... GABAA receptor antagonists, inverse agonists or negative allosteric modulators Bemegride Bicuculline Cicutoxin Cyclothiazide ...
Carisoprodol
... bemegride). Total amnesia of the experience is not uncommon following recovery.[citation needed] In 2014 actress Skye McCole ...
GABAA receptor negative allosteric modulator
Other GABAA NAMs, mostly non-selective, include amentoflavone, bemegride, bilobalide, cicutoxin, dieldrin, FG-7142, fipronil, ... and yet other GABAA receptor NAMs like bemegride, flurothyl, and pentylenetetrazol are used for clinical purposes. GABAA ...
List of MeSH codes (D03)
... bemegride MeSH D03.383.725.791.496 - iodopyridones MeSH D03.383.725.791.496.371 - iodopyracet MeSH D03.383.725.791.496.750 - ...
Causes of seizures
... bemegride, flumazenil, cyclothiazide, flurothyl, pentylenetetrazol, bicuculline, cicutoxin, and picrotoxin. There are varying ...
C8H13NO2
The molecular formula C8H13NO2 (molar mass: 155.19 g/mol, exact mass: 155.0946 u) may refer to: Arecoline Bemegride Scopine ...
Methyprylon
Pyrithyldione Piperidione Bemegride Thalidomide Glutethimide Phenglutarimide Ethchlorvynol US granted 2680116, Frick H, Lutz AH ...
Desbutal
These drugs often included picrotoxin, amiphenazole (Daptazile), bemegride (Megimide), and methamphetamine sulfate (Methedrine ...
ATC code R07
... phospholipids R07AA30 Combinations R07AB01 Doxapram R07AB02 Nikethamide R07AB03 Pentetrazol R07AB04 Etamivan R07AB05 Bemegride ...
List of drugs: Be
... bemegride (INN) bemesetron (INN) bemetizide (INN) Bemitradine (INN) Bemoradan (INN) Bemote Bemotrizinol (USAN) Ben-Allergin-50 ...
Bemegride
... (trademarked as Megimide) is a central nervous system stimulant. The drug was first made in 1911. It has been used in ... Definition: bemegride from Online Medical Dictionary Cullen, Pamela V., A Stranger in Blood: The Case Files on Dr John Bodkin ... Bemegride is also used to induce convulsions in experimental animals. The original synthesis involves first the condensation of ... Hullett took an overdose of barbiturates on 19 July 1956 but Adams only gave her a single 10cc dose of bemegride three days ...
GABRA4
Gamma-aminobutyric acid receptor subunit alpha-4 is a protein that in humans is encoded by the GABRA4 gene.[5][6] GABA is the major inhibitory neurotransmitter in the mammalian brain where it acts at GABA-A receptors, which are ligand-gated chloride channels. Chloride conductance of these channels can be modulated by agents such as benzodiazepines that bind to the GABA-A receptor. At least 16 distinct subunits of GABA-A receptors have been identified.[6] ...
Yohimbine
In the US, "yohimbe" preparations are sold as a dietary supplements for enhancing libido, for weight loss and as aids for bodybuilding; but "There is virtually no published research on yohimbe which supports these or any other claims".[9]:861 Often, these products explicitly claim to contain yohimbine.[8] Cohen et al. found that samples of brands sold in American brick-and-mortar stores contained highly variable amounts of yohimbine, and sometimes none at all.[8]:368 Labelling claims were often misleading.[8]:368 Similar results have been reported by other laboratories for products sold in the U.S., in other countries and on the internet.[15][16][17][18][19] One study found that many brands of "yohimbe" might not derive from the P. johimbe tree in the first place.[20] According to yet another source the yohimbe sold in markets in West Africa, where the tree grows, is frequently adulterated with other species of the genus Pausinystalia; these contain little yohimbine.[21] The amounts of alkaloid ...
A-366,833
Ji, Jianguo; Bunnelle, William H.; Anderson, David J.; Faltynek, Connie; Dyhring, Tino; Ahring, Philip K.; Rueter, Lynne E.; Curzon, Peter; Buckley, Michael J.; Marsh, Kennan C.; Kempf-Grote, Anita; Meyer, Michael D. (2007). "A-366833: A novel nicotinonitrile-substituted 3,6-diazabicyclo[3.2.0]-heptane α4β2 nicotinic acetylcholine receptor selective agonist: Synthesis, analgesic efficacy and tolerability profile in animal models". Biochemical Pharmacology. 74 (8): 1253-1262. doi:10.1016/j.bcp.2007.08.010. PMID 17854775 ...
4-Benzylpiperidine
... is a drug and research chemical used in scientific studies. It acts as a monoamine releasing agent with 20- to 48-fold selectivity for releasing dopamine versus serotonin. It is most efficacious as a releaser of norepinephrine, with an ec50 of 109/41.4/5246nM for DA/NE/5HT, respectively .[1] It has a fast onset of action and a short duration.[1] It also functions as a monoamine oxidase inhibitor (MAOI) with preference for MAO-A.[2] ...
RTI-229
... , also known as (-)-3β-(4-iodophenyl)tropane-2β-pyrrolidine carboxamide and RTI-4229-229, is a potent and long-lasting stimulant drug which was developed in the 1990s as part of a large group of related analogues from the phenyltropane family. With the combination of two potent dopamine transporter (DAT) binding motifs attached to the tropane ring, the p-iodophenyl group at the 3β-position and a pyrrolidine carboxamide at 2β, RTI-229 has extremely high selectivity for the dopamine transporter (2600x and 4600x selective over NET and 5-HTT respectively) and is one of the most DAT-selective compounds in the RTI series.[1][2] ...
Stimulant
Caffeine is a stimulant compound belonging to the xanthine class of chemicals naturally found in coffee, tea, and (to a lesser degree) cocoa or chocolate. It is included in many soft drinks, as well as a larger amount in energy drinks. Caffeine is the world's most widely used psychoactive drug and by far the most common stimulant. In North America, 90% of adults consume caffeine daily.[63] A few jurisdictions restrict its sale and use. Caffeine is also included in some medications, usually for the purpose of enhancing the effect of the primary ingredient, or reducing one of its side-effects (especially drowsiness). Tablets containing standardized doses of caffeine are also widely available. Caffeine's mechanism of action differs from many stimulants, as it produces stimulant effects by inhibiting adenosine receptors.[64] Adenosine receptors are thought to be a large driver of drowsiness and sleep, and their action increases with extended wakefulness.[65] Caffeine has been found to increase ...
Eugeroic
... s (originally, "eugrégorique" or "eugregoric"),[1] also known as wakefulness-promoting agents and wakefulness-promoting drugs, are a class of drugs that promote wakefulness and alertness.[2][3] They are medically indicated for the treatment of certain sleep disorders including excessive daytime sleepiness (EDS) in narcolepsy or obstructive sleep apnea (OSA).[2][3] They generally have a very low addictive potential.[2][3] Eugeroics are also often prescribed off-label for the treatment of EDS in idiopathic hypersomnia,[4] a rare and often debilitating sleep disorder which currently has no official treatments approved by the Food and Drug Administration (FDA). Modafinil and armodafinil each act as a selective, weak, atypical dopamine reuptake inhibitor (DRI)[2][3] whereas adrafinil acts as a prodrug for modafinil. Other eugeroics include solriamfetol, which acts as a norepinephrine-dopamine reuptake inhibitor (NDRI), and pitolisant, which acts as a histamine 3 (H₃) receptor ...
3-Fluoromethcathinone
... (also known as 3-FMC) is a chemical compound of the phenethylamine, amphetamine, and cathinone classes that has been sold online as a designer drug.[1][2] It is a structural isomer of flephedrone (4-fluoromethcathinone). 3-Fluoroisomethcathinone is produced as a by-product when 3-FMC is synthesized, the activity of this compound is unknown.[3] ...
Naphyrone
... emerged as a new legal high in the United Kingdom only months after the ban of similar drug mephedrone (which was also a cathinone derivative). Until July 2010 the substance was not controlled by the Misuse of Drugs Act 1971 and was therefore not illegal for someone to possess. The Medicines Act prevented naphyrone from being sold for human consumption, and therefore it was sometimes sold as 'pond cleaner' or as another substance not normally consumed by humans. In response to this emerging trend of new designer drugs, Home Office Minister James Brokenshire said, "action to address the issue of emerging legal highs coming on to the market is a priority for the government."[12][unreliable source?] A study by researchers at Liverpool John Moores University found that only one out of ten products labelled as "NRG-1" actually contained naphyrone when they were subjected to laboratory analysis. Compounds found in products labelled NRG-1 included MDPV, flephedrone, mephedrone, butylone and ...
Hexacyclonate
... (Gevilon) is a stimulant drug. It has been used for the treatment of alcoholism[1] and for increasing motivation in elderly patients,[2] but is now mainly used for the treatment of hyperlipoproteinaemia. [3][4] It is chemically similar to the anticonvulsant gabapentin, with a hydroxyl group replacing the amine. The latter use may be incorrectly assigned, as "Gevilon" has been used as a trade name for gemfibrozil, a well-known drug for dislypidemia. ...
Syrup of ipecac
Ipecac was used in cough mixtures as an expectorant or an emetic from the 18th until the early 20th century.[citation needed] For instance, Ipecac and opium were used to produce Dover's powder, which was used in syrup form.[citation needed] In 1965, the FDA approved the sale of up to one ounce of syrup of ipecac without a prescription. At the time it was approved, its use was recommended by the AAP, AAPCC, AMA, and the FDA's medical advisory board as a method to induce vomiting "for quick first-aid use in the home, under medical supervision", for use in cases of accidental poisoning.[2][3] Current guidelines from the American Academy of Pediatrics, however, strongly advise against this and in fact recommend the disposal of any syrup of ipecac present in the home.[4] Many toxicological associations have also issued position papers recommending against its use as a first-line treatment for most ingested poisons,[5] because of a lack of evidence that syrup of ipecac actually helps improve the ...
Nalorphine dinicotinate
... (trade name Nimelan), also known as N-allylnormorphine dinicotinate, dinicotinoylnalorphine, or niconalorphine, is a semisynthetic, mixed opioid agonist-antagonist which is described as a narcotic antagonist but may produce limited analgesia and sedation at higher doses in opioid naive patients (with limited euphoria and dependence liability).[1][2] It is the 3,6-dinicotinate ester of nalorphine, and is therefore the nalorphine analogue of nicomorphine (which is the 3,6-dinicotinate ester of morphine). As nalorphine dinicotinate is only regulated at the Rx (prescription required) drug, it would be legal to possess with a valid prescription should a patient manage to acquire it.[citation needed] ...
Cysteine
In the translation of messenger RNA molecules to produce polypeptides, cysteine is coded for by the UGU and UGC codons. Cysteine has traditionally been considered to be a hydrophilic amino acid, based largely on the chemical parallel between its sulfhydryl group and the hydroxyl groups in the side chains of other polar amino acids. However, the cysteine side chain has been shown to stabilize hydrophobic interactions in micelles to a greater degree than the side chain in the nonpolar amino acid glycine and the polar amino acid serine.[19] In a statistical analysis of the frequency with which amino acids appear in different chemical environments in the structures of proteins, free cysteine residues were found to associate with hydrophobic regions of proteins. Their hydrophobic tendency was equivalent to that of known nonpolar amino acids such as methionine and tyrosine (tyrosine is polar aromatic but also hydrophobic[20]), those of which were much greater than that of known polar amino acids such ...
Acetylcysteine
Intravenous and oral formulations of acetylcysteine are available for the treatment of paracetamol (acetaminophen) overdose.[13] When paracetamol is taken in large quantities, a minor metabolite called N-acetyl-p-benzoquinone imine (NAPQI) accumulates within the body. It is normally conjugated by glutathione, but when taken in excess, the body's glutathione reserves are not sufficient to deactivate the toxic NAPQI. This metabolite is then free to react with key hepatic enzymes, thereby damaging liver cells. This may lead to severe liver damage and even death by acute liver failure. In the treatment of acetaminophen overdose, acetylcysteine acts to maintain or replenish depleted glutathione reserves in the liver and enhance non-toxic metabolism of acetaminophen.[14] These actions serve to protect liver cells from NAPQI toxicity. It is most effective in preventing or lessening hepatic injury when administered within 8-10 hours after overdose.[14] Research suggests that the rate of liver toxicity ...
2-Fluoroamphetamine
... (2-FA) is a stimulant drug from the amphetamine family which has been sold as a designer drug.[1] 2-Fluoroamphetamine differs from 3- and 4-fluoroamphetamine in the position of the fluorine atom on the aromatic ring, making them positional isomers of one another. The replacement of a hydrogen atom with a fluorine atom in certain compounds to facilitate passage through the blood-brain barrier, as is desirable in central nervous system pharmaceutical agents, is a common practice due to the corresponding increase in lipophilicity granted by the substitute.[2][3] ...
Bemegride - Wikipedia
Bemegride (trademarked as Megimide) is a central nervous system stimulant. The drug was first made in 1911. It has been used in ... Definition: bemegride from Online Medical Dictionary Cullen, Pamela V., A Stranger in Blood: The Case Files on Dr John Bodkin ... Bemegride is also used to induce convulsions in experimental animals. The original synthesis involves first the condensation of ... Hullett took an overdose of barbiturates on 19 July 1956 but Adams only gave her a single 10cc dose of bemegride three days ...
Bemegride in Barbiturate Poisoning Complicated by Alcohol | The BMJ
Bemegride | C8H13NO2 | ChemSpider
Bemegride is a central nervous system stimulant and antidote for barbiturate poisoning.;Target: GABAA receptor Bemegride has an ... Bemegride is a central nervous system stimulant and antidote for barbiturate poisoning.; target: GABAA receptor ; Bemegride has ... Bemegride is a central nervous system stimulant and antidote for barbiturate poisoning. MedChem Express ... 1] Long-term oral administration to the rat of barbitone, alone or together with the analeptics bemegride or pentylenetetrazol ...
Bemegride
Summary Report | CureHunter
Bemegride: A CNS stimulant that is used to induce convulsions in experimental animals. It has also been used as a respiratory ... Bemegride. Subscribe to New Research on Bemegride A CNS stimulant that is used to induce convulsions in experimental animals. ... 10/01/2006 - "Although a bemegride-induced seizure arose from the right side during the subdural recording, the onset of 5 ... 03/01/2009 - "The present case suggested that bemegride is one of the alternative measures in patients with poor seizure ...
Butalbital-D5 (0.1 mg/ml) in Methanol- CAS Number 145243-96-5
R)-(-)-Bromo-DragonFLY HCl (1.0 mg/mL) (as free base) in Methanol- CAS Number 332012-24-5
Questions & Answers
Acute intermittent porphyria (AIP) is one of the porphyrias, a group of diseases involving defects in heme metabolism and that results in excessive secretion of porphyrins and porphyrin precursors. AIP manifests itself by abdomen pain, neuropathies, and constipation, but, unlike most types of porphyria, patients with AIP do not have a rash.
Hereditary Coproporphyria Treatment & Management: Approach Considerations, Diet
Patent US5413996 - Targeted drug delivery via phosphonate derivatives - Google Patents
Effect of colour of drugs: systematic review of perceived effect of drugs and of their effectiveness | The BMJ
Amiphenazole - Wikipedia
Rowell NR (February 1957). "Treatment of glutethimide poisoning with bemegride and amiphenazole". Lancet. 272 (6965): 407-9. ... usually in combination with bemegride,[1][2] as well as poisoning from other sedative drugs[3][4] and treatment of respiratory ... "Treatment of acute primidone poisoning with bemegride and amiphenazole". British Medical Journal. 2 (5042): 451-2. doi:10.1136 ... "Barbiturate poisoning treated with amiphenazole and bemegride". British Medical Journal. 2 (5001): 1099-101. doi:10.1136/bmj. ...
GABA Receptors - Neuronal Signaling
GABRA1 Gene - GeneCards | GBRA1 Protein | GBRA1 Antibody
Modafinil
Federal Register
::
Schedules of Controlled Substances: Placement of Carisoprodol Into Schedule IV
Medicine/First Aid/Materials - Wikiversity
ATC code R07 - wikidoc
Primidone - Wikipedia
Treatments for primidone overdose have included hemoperfusion with forced diuresis,[48] a combination of bemegride and ... "Treatment of Acute Primidone Poisoning with Bemegride and Amiphenazole". British Medical Journal. 2 (5042): 451-2. doi:10.1136 ... amiphenazole;[51] and a combination of bemegride, spironolactone, caffeine, pentylenetetrazol, strophanthin, penicillin and ...
CAS # 64-65-3, Bemegrid, 4-Ethyl-4-methyl-2,6-piperidinedione, 4-Methyl-4-ethyl-2,6-dioxopiperidine, Agipnon, Ahypnon,...
National Drug Schedules | NAPRA
DailyMed - BENZTROPINE MESYLATE injection
2011 - Final Rule: Placement of Carisoprodol Into Schedule IV
Bemegride fully blocked the discriminative stimulus effects of the training dose of carisoprodol (100 mg/kg p.o.), whereas the ... 5), found that 5 mg/kg bemegride antagonized the discriminative stimulus effects produced by 100 mg/kg of carisoprodol in rats ... Jasinski further opined that the finding that bemegride, a non-specific barbiturate antagonist, apparently reduced the amplit[ ... In a further study, bemegride, a barbiturate antagonist, antagonized the discriminative stimulus effect of carisoprodol in rats ...
Poisons Act (Amendment of Schedule) Notification 1997 - Singapore Statutes Online
List Of Chemical Antidotes
GABA阻害 | GABA受容体活性化 | GABA Receptor Inhibition
GABA Receptors - Neuronal | 神经信号通路
National Ambulatory Medical Care Survey, 1994
Code System Concept
Iodohippurate in English with contextual examples
Megimide1
- Bemegride (trademarked as Megimide) is a central nervous system stimulant. (wikipedia.org)
Analeptics bemegride2
- 1] Long-term oral administration to the rat of barbitone, alone or together with the analeptics bemegride or pentylenetetrazol, show that the intensity of the withdrawal syndrome generally parallels the degree of associated CNS depression. (chemspider.com)
- Analeptics (bemegride, corazol, etc., see Chapter 12) prescribed only in mild forms of poisoning, in severe poisoning they not only contribute to the restoration of respiration, but can even worsen the condition of the patient. (hindimequotes.com)
Central nervous system s1
- Bemegride is a central nervous system stimulant and antidote for barbiturate poisoning. (chemspider.com)
Flumazenil1
- Gastric lavage, administration of flumazenil and bemegride may be effective for acute intoxication case. (criticalcareshock.org)
Cases1
- In most cases, bemegride). (languagewriting.com)
Action1
- Bemegride has an antagonistic action on the GABAA receptor, suppressing both GABA- and pentobarbitone-evoked whole-cell currents to similar extents. (chemspider.com)
Treatment1
- Hullett took an overdose of barbiturates on 19 July 1956 but Adams only gave her a single 10cc dose of bemegride three days later on the 22nd, despite having acquired 100cc for her treatment. (wikipedia.org)