A centrally acting muscarinic antagonist. Benactyzine has been used in the treatment of depression and is used in research to investigate the role of cholinergic systems on behavior.
A broad category of chemical actions and uses that result in the prevention, treatment, cure or diagnosis of disease. Included here are drugs and chemicals that act by altering normal body functions, such as the REPRODUCTIVE CONTROL AGENTS and ANESTHETICS. Effects of chemicals on the environment are also included.
One of the MUSCARINIC ANTAGONISTS with pharmacologic action similar to ATROPINE and used mainly as an ophthalmic parasympatholytic or mydriatic.
Agents that dilate the pupil. They may be either sympathomimetics or parasympatholytics.
Drugs that bind to but do not activate MUSCARINIC RECEPTORS, thereby blocking the actions of endogenous ACETYLCHOLINE or exogenous agonists. Muscarinic antagonists have widespread effects including actions on the iris and ciliary muscle of the eye, the heart and blood vessels, secretions of the respiratory tract, GI system, and salivary glands, GI motility, urinary bladder tone, and the central nervous system.
The aperture in the iris through which light passes.
A parasympatholytic anticholinergic used solely to obtain mydriasis or cycloplegia.
Databases devoted to knowledge about specific chemicals.
It is a form of protection provided by law. In the United States this protection is granted to authors of original works of authorship, including literary, dramatic, musical, artistic, and certain other intellectual works. This protection is available to both published and unpublished works. (from Circular of the United States Copyright Office, 6/30/2008)
The interchange of goods or commodities, especially on a large scale, between different countries or between populations within the same country. It includes trade (the buying, selling, or exchanging of commodities, whether wholesale or retail) and business (the purchase and sale of goods to make a profit). (From Random House Unabridged Dictionary, 2d ed, p411, p2005 & p283)
A basis of value established for the measure of quantity, weight, extent or quality, e.g. weight standards, standard solutions, methods, techniques, and procedures used in diagnosis and therapy.
Individuals responsible for various duties pertaining to the medical office routine.
An oxidation product of HEPTACHLOR formed by many plants and animals, including humans, after exposure to HEPTACHLOR. It has been shown to remain in soil treated with HEPTACHLOR for over fifteen years and is toxic to animals and humans. (From ATSDR Public Heath Statement, April 1989)
A highly poisonous substance that was formerly used as an insecticide. The manufacture and use has been discontinued in the U.S. (From Merck Index, 11th ed)
Software used to locate data or information stored in machine-readable form locally or at a distance such as an INTERNET site.
The largest country in North America, comprising 10 provinces and three territories. Its capital is Ottawa.
Drugs that cannot be sold legally without a prescription.
Works about lists of drugs or collections of recipes, formulas, and prescriptions for the compounding of medicinal preparations. Formularies differ from PHARMACOPOEIAS in that they are less complete, lacking full descriptions of the drugs, their formulations, analytic composition, chemical properties, etc. In hospitals, formularies list all drugs commonly stocked in the hospital pharmacy.
A component of the Executive Office of the President established by the Anti-Drug Abuse Act of 1988. The Office establishes policies, priorities, and objectives for national DRUG AND NARCOTIC CONTROL. The goals of the program are to reduce illicit drug use, manufacturing, and trafficking, drug-related crime and violence, and drug-related health consequences.
Drugs considered essential to meet the health needs of a population as well as to control drug costs.
Component of the NATIONAL INSTITUTES OF HEALTH. It supports a comprehensive research portfolio that focuses on the biological, social, behavioral and neuroscientific bases of drug abuse on the body and brain as well as its causes, prevention, and treatment. NIDA, NIAAA, and NIMH were created as coequal institutes within the Alcohol, Drug Abuse and Mental Health Administration in 1974. It was established within the NATIONAL INSTITUTES OF HEALTH in 1992.
Substances that induce LACTATION.
Disorders in which the symptoms are distressing to the individual and recognized by him or her as being unacceptable. Social relationships may be greatly affected but usually remain within acceptable limits. The disturbance is relatively enduring or recurrent without treatment.
A plant genus in the family PAPAVERACEAE, order Papaverales, subclass Magnoliidae.
Drugs used to induce drowsiness or sleep or to reduce psychological excitement or anxiety.
Keto-pyrans.
Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, and practicability of these interventions in individual cases or series.
Physiological and psychological symptoms associated with withdrawal from the use of a drug after prolonged administration or habituation. The concept includes withdrawal from smoking or drinking, as well as withdrawal from an administered drug.
An eleven-amino acid neurotransmitter that appears in both the central and peripheral nervous systems. It is involved in transmission of PAIN, causes rapid contractions of the gastrointestinal smooth muscle, and modulates inflammatory and immune responses.

Drug-induced changes in brain acetylcholine. (1/4)

In rats, drug-induced depression of the central nervous system has been shown generally to be associated with an elevation in level of total acetylcholine in the brain. This generalization held true for a wide variety of depressant drugs with one notable exception: the subacute administration of reserpine, with which there was an increase in cerebral acetylcholine after the first dose, but a return to normal levels after subsequent doses, despite continued depression of the animals. Reduction in the level of total acetylcholine in the brain followed the administration of certain convulsants (pentylenetetrazole and 3,5-dimethylbutylethylbarbiturate); but no change was seen after the administration of several mildly exciting agents. The notable exceptions to this generalization were atropine and scopolamine, which significantly lowered brain acetylcholine in doses producing mild excitation in only some of the animals and no gross manifestations in the rest.  (+info)

Effect of chlorpromazine, reserpine, benactyzine and phenobarbitone on the release of corticotrophin in the rat. (2/4)

A single injection into the rat of chlorpromazine, reserpine, benactyzine or phenobarbitone stimulates the release of corticotrophin. This effect is not seen after the drugs have been injected daily for 5 days, nor when the rats are hypophysectomized or pretreated with hydrocortisone. The stimulant effect of ether on corticotrophin release is not modified by pretreatment with a single injection, nor to any great extent after 5 daily injections of these drugs.  (+info)

SOME ACTIONS OF CENTRALLY ACTIVE AND OTHER DRUGS ON THE TRANSMISSION OF SINGLE NERVE IMPULSES THROUGH THE ISOLATED SUPERIOR CERVICAL GANGLION PREPARATION OF THE RABBIT. (3/4)

The effect of some centrally-active and other drugs on the transmission of single nerve impulses through the isolated superior cervical ganglion preparation of the rabbit has been studied by recording both preganglionic and postganglionic action potentials. Block of conduction in the axon could be distinguished from block of the synaptic mechanism. The drugs did not appear to exert any one characteristic form of blocking action. A continuous spectrum of drug action linked an agent such as meprobamate which acted predominantly on the synapse to benactyzine which acted mainly by blocking axonal conduction. The drugs have been divided into three groups. Group I: hexamethonium, meprobamate, paraldehyde, amylobarbitone, methylpentynol and azacyclonal; these acted relatively selectively at the ganglion. Group II: N714C (the cis-isomer of chlorprothixene), prochlorperazine, methylpentynol carbamate, pipradrol, promethazine, perphenazine and procaine; the action of these drugs on the ganglion could be accounted for entirely in terms of their axonal depressant action. Group III: chlorprothixene, promazine, N720 (dihydrochlorprothixene), chlorpromazine, hydroxyzine and benactyzine; these drugs also blocked axonal conduction but in addition they appeared to exert a "facilitating" action at the ganglionic synapse. The actions of adrenaline, adrenochrome, iproniazid, ergotoxine, mescaline and lysergic acid diethylamide on transmission were also studied. The implications of the modifications of ganglionic transmission produced by these drugs is discussed.  (+info)

THE SELECTIVITY OF DRUGS BLOCKING GANGLIONIC TRANSMISSION IN THE RAT. (4/4)

By comparing the effects on ganglionic transmission and on the pre- and post-ganglionic nerves in the isolated superior cervical ganglion preparation of the rat, the selectivity of several drugs was assessed quantitatively. Hexamethonium, tetraethylammonium, nicotine and tubocurarine blocked transmission in concentrations which did not affect nervous conduction and were considered to be highly selective in action. Atropine, amylobarbitone and paraldehyde depressed nervous conduction appreciably in ganglion-blocking doses, but not enough to account wholly for the block in transmission and they were therefore considered as being moderately selective. The ganglion blocking actions of mephenesin, procaine, methylpentynol, methylpentynol carbamate and benactyzine were nonspecific, showing general depression of neuronal activity. Ganglion block with bretylium was nonselective in its site of depression of the postganglionic neurone in concentrations which only partly depressed the preganglionic nerve.  (+info)

Benactyzine: A centrally acting muscarinic antagonist. Benactyzine has been used in the treatment of depression and is used in research to investigate the role of cholinergic systems on behavior.
Gery, I and Eidinger, D, Selective and opposing effects of cytochalasin b and other drugs on lymphocyte responses to different doses of mitogens. (1977). Subject Strain Bibliography 1977. 3098 ...
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Subjects. These experiments were done on ∼200 wild-type Aplysia californica, weighing 250-350 gm (Marinus, Long Beach, CA). The animals were maintained at 14-16°C in holding tanks containing aerated, filtered artificial seawater (ASW) for 3-6 d before being used for experiments.. Preparations. Three types of preparations were used: an isolated ganglia preparation, a semi-intact (isolated head) preparation, and a reduced preparation. Before dissection, the animal was immobilized by an injection of an isotonic magnesium chloride solution of ∼25% of body volume.. The isolated ganglia preparation included all the head ganglia (buccal, cerebral, pedal, and pleural). In some experiments, as specified, we also included the abdominal ganglion or pedal arteries. All ganglia, except the buccal, were pinned dorsal side up to a clear Sylgard silicone elastomer floor of a recording chamber containing fresh ASW. The buccal ganglion was pinned rostral surface up. For the preparations of head ganglia with ...
Physicists have worked out how to measure the magnetic fields generated by single nerves from outside the body and at room temperature.
FARGO, N.D. (AP) - Federal authorities unsealed indictments Monday against 22 people charged with conspiracy to sell heroin and other drugs on an Indian re
Britains top share index touched a session high as chancellor Philip Hammond delivered his budget statement on Wednesday, boosted by a dip in sterling as Brexit-bound Britain slashed economic growth forecasts. Housebuilding stocks swung sharply, losing ground after Hammond announced a review of
The effect of guanidine on neuromuscular transmission was studied in the sciatic-sartorius preparation of the frog, using intracellular electrodes. The sensitivity of the ned-plate to ACh was measured by applying ACh electrophoretically. Guanidine was also applied in the same way.. Guanidine greatly increased the amplitude of e.p.p. of curarized muscle without changing the resting potential at the end-plate region. Guanidine exhibited no effect on the cholinesterase activity, and it did not change the sensitivity of the end-plate to ACh. It is concluded that the drug increases the amplitude of e.p.p. by increasing the quantity of ACh released from the nerve ending by a single nerve impulse.. Membrane potential was recorded from endplates of guanidine-treated nerve-muscle preparation showing spontaneous twitchings. The most striking event was the appearance of spontaneous e.p.p.s of more than 5 mV size (giant potential), some of which did not reach threshold the others elicited the conducted ...
TY - JOUR. T1 - Patterns of brain acetylcholine release predict individual differences in preferred learning strategies in rats. AU - McIntyre, Christa K.. AU - Marriott, Lisa K.. AU - Gold, Paul E.. PY - 2003/3/1. Y1 - 2003/3/1. N2 - Acetylcholine release was measured simultaneously in the hippocampus and dorsal striatum of rats before and during training on a maze that could be learned using either a hippocampus-dependent spatial strategy or a dorsal striatum-dependent turning strategy. A probe trial administered after rats reached a criterion of 9/10 correct responses revealed that about half of the rats used a spatial strategy and half a turning strategy to solve the task. Acetylcholine release in the hippocampus, as well as the ratio of acetylcholine release in the hippocampus vs. the dorsal striatum, measured either before or during training, predicted these individual differences in strategy selection during learning. These findings suggest that differences in release of acetylcholine ...
7.1 Impact of Other Drugs on Amlodipine 7.2 Impact of Amlodipine on Other Drugs . 8 USE IN SPECIFIC POPULATIONS . 8.1 Pregnancy . 8.2 Lactation 8.4 Pediatric Use . 8.5 Geriatric Use 8.6 Hepatic Impairment . 10 OVERDOSAGE 11 DESCRIPTION 12 CLINICAL PHARMACOLOGY . 12.1 . Mechanism of Action 12.2 . Pharmacodynamics 12.3 . Pharmacokinetics . 13
Methamphetamines are in a class of drugs which are termed central nervous system stimulants. This places them in the same class as cocaine, PCP, ecstasy and the newest scourge on the markets, Bath Salts. This classification of drugs causes people to feel more awake and stimulated. The difference is that Meth is like these other drugs on steroids! Methamphetamines cause the following effects on the human body:. Destructive lifestyle. Methamphetamine, popularly shortened to meth and also nicknamed ice or Speed, is addictive. In other words it produces an initial pleasurable effect, followed by a rebound unpleasant effect. It starts with an up and is followed by an unpleasant down which can be avoided by taking more of the drug. The longer the up is maintained, the worse the down feels, and the harder the addict will seek the drug to maintain the high. The harder the addict seeks the drug, the less attention he/she pays to his/her other bodily needs. Addicts stop caring for ...
Pull some of the wires out of the cord and separate them so the child can see that its not just one single wire inside the cord. Explain that is similar to the nerves in our body. And just like the cord needs every single wire to operate properly, our bodies need every single nerve to fully function. Any nerve that is damaged will create some kind and level of difficulty for our body. ...
FISH is a taxonomic staining method in which fluorescent DNA probes hybridise to ribosomal RNA in whole cells. FISH is culture independent and the test can be completed within 24 hours. T(D)GGE is a gel-electrophoretic separation procedure for double stranded deoxyribonucleic acids (dsDNA) produced by primer directed DNA amplification. T(D)GGE is a very useful method in order to monitor the effect of probiotics and antibiotics as well as other drugs on the intestinal microflora of human and animals. Also real time PCR can be used to monitor and quantify the presence of specific bacteria or even genes in the gut flora ...
Bodur E, Cokuğraş AN, Tezcan EF (February 2001). "Inhibition effects of benactyzine and drofenine on human serum ...
Treatment for poisoning with GV involves drugs such as atropine, benactyzine, obidoxime, and HI-6. Fluorotabun ...
... closely related to benactyzine (an anticholinergic). Further, the structure is similar to methadone and related compounds like ...
... benactyzine Tricycle: amitriptyline, melitracen, cyclobenzaprine, tianeptine, amineptine, clopenthixol, chlorprothixene, ...
The molecular formula C20H25NO3 (molar mass: 327.42 g/mol) may refer to: Benactyzine, an antidepressant Difemerine, an ...
Benactyzine EA 2148-A - Phencyclidine (PCP) EA 2233 - A dimethylheptylpyran variant Eight individual isomers numbered EA-2233-1 ...
... benactyzine MeSH D02.241.511.085.740 - quinuclidinyl benzilate MeSH D02.241.511.316 - glycolates MeSH D02.241.511.316.300 - 2,4 ... benactyzine MeSH D02.241.223.601.238.306.740 - quinuclidinyl benzilate MeSH D02.241.223.601.329 - guanfacine MeSH D02.241. ...
Benactyzine EA 2148-A - Phencyclidine (PCP) EA 2233 - A dimethylheptylpyran variant Eight individual isomers numbered EA-2233-1 ...
Ben-Allergin-50 Injection Ben-Aqua Bena-D benactyzine (INN) Benadryl (Johnson & Johnson) benafentrine (INN) benaprizine (INN) ...
InChI=1S/C26H37NO3/c1-18(2)26(29)30-25-13-12-21(17-28)16-24(25)23(22-10-8-7-9-11-22)14-15-27(19(3)4)20(5)6/h7-13,16,18-20,23,28H,14-15,17H2,1-6H3/t23-/m1/s1 ...
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There are a variety of clinically useful ergoline derivatives for the purpose of vasoconstriction, the treatment of migraines, and treatment of Parkinson's disease. Ergoline alkaloids found their place in pharmacology long before modern medicine as preparations of ergot were often used by midwives in the 12th century to stimulate childbirth.[10] Following Arthur Stoll's isolation of ergometrine, the therapeutic use of ergoline derivatives became well explored. The induction of uterine contractions via the preparation of ergot was attributed to ergonovine, an ergoline derivative found in ergot, which is a powerful oxytocic. From this, methergine, a synthetic derivative, was elucidated.[7] While used to facilitate child birth, ergoline derivatives can pass into breast milk and should not be used during breastfeeding.[11] They are uterine contractors that can increase the risk of miscarriage during pregnancy.[3] Another example of medically relevant ergoline alkaloids is ergotamine, an alkaloid ...
Used in fixed combination with chlordiazepoxide as adjunctive therapy in the treatment of peptic ulcer disease; however, no conclusive data that antimuscarinics aid in the healing, decrease the rate of recurrence, or prevent complications of peptic ulcers.[2] With the advent of more effective therapies for the treatment of peptic ulcer disease, antimuscarinics have only limited usefulness in this condition. ...
... poisoning is characterized by miosis, blurred vision, increased salivation, excessive sweating, lacrimation, bronchial secretions, bronchoconstriction, bradycardia, abdominal cramping, increased gastric acid secretion, diarrhea and polyuria. If muscarine reaches the brain it can cause tremor, convulsions and hypothermia. Cardiac ventricles contain muscarinic receptors that mediate a decrease in the force of contractions leading to a lower blood pressure. If muscarine is administered intravenously, muscarine can trigger acute circulatory failure with cardiac arrest.[1] The symptoms of intoxication with mushrooms rich in muscarine, especially Inocybe, are very typical: The symptoms start early, after one-quarter to two hours, with headache, nausea, vomiting, and constriction of the pharynx. Then salivation, lacrimation, and diffuse perspiration set in, combined with miosis, disturbed accommodation, and reduced vision. Gastric and small bowel colic leads to diarrhea, and there is a ...
... (LA-SS-Az, LSZ) is an analog of LSD developed by the team led by David E. Nichols at Purdue University.[1][2] It was developed as a rigid analog of LSD with the diethylamide group constrained into an azetidine ring in order to map the binding site at the 5-HT2A receptor. There are three possible stereoisomers around the azetidine ring, with the (S,S)-(+) isomer being the most active, slightly more potent than LSD itself in drug discrimination tests using trained rats.[3] There have been several unconfirmed reports of lysergic acid 2,4-dimethylazetidide being synthesized in illicit laboratories and distributed on blotter paper or in liquid solution under names such as "diazedine" and "λ".[4][5] In 2013 LSZ also appeared on some designer drug and research chemical markets in the UK.[6][unreliable source?][7] LSZ later gained international popularity through a small cluster of mail-order novel psychedelic shops that appeared in 2012.[8] ...
... (DOPR) is a psychedelic drug of the phenethylamine and amphetamine chemical classes. It was first synthesized by Alexander Shulgin, and was described in his book PiHKAL (Phenethylamines i Have Known And Loved). Shulgin described DOPR is a "heavy duty psychedelic", complete with alterations of the thought process and visual distortion.[1] Very little data exists about the pharmacological properties, metabolism, and toxicity of DOPR. The alternative structural isomer DOIP, with a 4-isopropyl substitution, is also known but is around ten times weaker than DOPR, with an active dose of some 20-30 mg (as compared to 2-5 mg for DOPR).[1] ...
... (acetyl coenzyme A) is a molecule that participates in many biochemical reactions in protein, carbohydrate and lipid metabolism.[1] Its main function is to deliver the acetyl group to the citric acid cycle (Krebs cycle) to be oxidized for energy production. Coenzyme A (CoASH or CoA) consists of a β-mercaptoethylamine group linked to the vitamin pantothenic acid through an amide linkage [2] and 3'-phosphorylated ADP. The acetyl group (indicated in blue in the structural diagram on the right) of acetyl-CoA is linked to the sulfhydryl substituent of the β-mercaptoethylamine group. This thioester linkage is a "high energy" bond, which is particularly reactive. Hydrolysis of the thioester bond is exergonic (−31.5 kJ/mol). CoA is acetylated to acetyl-CoA by the breakdown of carbohydrates through glycolysis and by the breakdown of fatty acids through β-oxidation. Acetyl-CoA then enters the citric acid cycle, where the acetyl group is oxidized to carbon dioxide and water, and the energy ...
... (5-bromo-N,N-dimethyltryptamine) is a psychedelic brominated indole alkaloid found in the sponges Smenospongia aurea and Smenospongia echina, as well as in Verongula rigida (0.00142% dry weight) alongside 5,6-Dibromo-DMT (0.35% dry weight) and seven other alkaloids.[1][2][3][4] It is the 5-bromo derivative of DMT, a psychedelic found in many plants and animals. 5-Bromo-DMT has a pEC50 value of 5.51 for the 5-HT2A receptor.[5] Animal studies on 5-Bromo-DMT showed that it produces effects suggestive of sedative and antidepressant activity and caused significant reduction of locomotor activity in the rodent FST model.[6] 5-Bromo-DMT was reported to be psychoactive at 20-50 mg via vaporization with mild psychedelic-like activity.[7] ...
... is a potent and long lasting anticholinergic deliriant drug, related to the chemical warfare agent 3-Quinuclidinyl benzilate (QNB). It was developed under contract to Edgewood Arsenal during the 1960s as part of the US military chemical weapons program, during research to improve upon the properties of earlier agents such as QNB. The main advantages of EA-3443 were not only increased potency over QNB, but also a significantly improved central to peripheral effects ratio. Anticholinergic drugs produce both incapacitating deliriant effects through action in the brain, and a variety of distinctive physical symptoms such as dry mouth, dilated pupils, blurred vision and hot flushed skin, all of which together comprise the "anticholinergic syndrome" which is generally easy for doctors to diagnose. EA-3443 however is mainly selective for the brain, and when administered in a narrow dose range of around 0.3mg can produce the central effects of confusion, hallucinations and amnesia, but without ...
Schedule I in Sweden. 2C-T-2 was first classified as "health hazard" under the act Lagen om förbud mot vissa hälsofarliga varor (translated Act on the Prohibition of Certain Goods Dangerous to Health) as of April 1, 1999, under SFS 1999:58[6] that made it illegal to sell or possess. The Riksdag added 2C-T-2 to Narcotic Drugs Punishments Act under Swedish schedule I ("substances, plant materials and fungi which normally do not have medical use") as of March 16, 2004, published by Medical Products Agency (MPA) in regulation LVFS 2004:3 listed as 2C-T-2, 2,5-dimetoxi-4-etyltiofenetylamin.[7] ...
In the United Kingdom, 2C-E is a Class A controlled substance. The UK has the strictest laws in the EU on designer drugs. The Misuse Of Drugs Act was amended in 2002 to include a "catch most" clause outlawing every drug, and possible future drug, from the LSD (ergoline) and MDMA (phenethylamine) chemical families (including 2C-E). The amendment is a near verbatim quote from the books of the American biochemist Alexander Shulgin, who obtained a PhD from the University of California, Berkeley. Dr. Shulgin, a former research chemist at the Dow Chemical Company, re-discovered the synthesis for MDMA in 1976 and published the syntheses for more than 200 phenethylamine compounds of his own invention, and 55 tryptamine compounds many of which were also his own invention. The Shulgins were motivated to release the synthesis information as a way to protect the public's access to information about psychedelic compounds, a goal Alexander Shulgin has noted many times. ...
Many users report degradation of alpha-GPC when stored openly or for long periods of time. Alpha-GPC is hygroscopic and will pull moisture in from the surrounding air. This will cause the powder to turn into what appears to be a gel. Alpha-GPC with ,99% purity will undergo this process at a visible rate (seconds to minutes) and thus requires minimized exposure to the air. This hygroscopic quality can cause gel capsules not fully packed with alpha-GPC to dissolve. Proper storage methods need to be used with alpha-GPC and include removing all air from the container, double bagging with plastic bags rated for chemicals (less likely to leak air), and storing bulk/excess inside the freezer. Vacuum sealed bags are highly recommended. For people accessing alpha-GPC daily it is advisable to separate a month's supply from excess and storing the excess as best as possible. Vacuum sealing a large supply into many 1 month dividends is a method positively reported by many users. It is important to note that ...
... (INN) (brand names Lethidrone, Nalline), also known as N-allylnormorphine, is a mixed opioid agonist-antagonist with opioid antagonist and analgesic properties.[1] It was introduced in 1954[2] and was used as an antidote to reverse opioid overdose and in a challenge test to determine opioid dependence.[3] It acts at two opioid receptors - the μ-opioid receptor (MOR) where it has antagonistic effects, and at the κ-opioid receptor (KOR) (Ki = 1.6 nM; EC50 = 483 nM; Emax = 95%) where it exerts high-efficacy partial agonist/near-full agonist characteristics.[4] Nalorphine was the second opioid antagonist to be introduced, preceded by nalodeine (N-allylnorcodeine) in 1915 and followed by naloxone in 1960 and naltrexone in 1963.[2] Due to potent activation of the KOR, nalorphine produces side effects such as dysphoria, anxiety, confusion, and hallucinations, and for this reason, is no longer used medically.[1][2][5] Nalorphine has a number of analogues including niconalorphine (the ...
... (JB-318) is an anticholinergic drug related to the chemical warfare agent 3-Quinuclidinyl benzilate.. N-Ethyl-3-piperidyl benzilate is less potent and shorter acting than 3-quinuclidyl benzilate, but like 3-QNB its effects on the central nervous system predominate over peripheral effects. It produces deliriant and hallucinogenic effects similar to those of plants such as datura and may be used recreationally at low doses; however, unpleasant side effects such as dysphoria, nausea and vomiting, dizziness and extreme dry mouth tend to make abuse of drugs of this kind uncommon. Both the N-methyl and N-ethyl analogues of 3-piperidyl benzilate are, however, Schedule I controlled drugs.. Radiolabelled versions of this drug have been used in scientific research to map the distribution of muscarinic acetylcholine receptors in the brain, however this drug has slightly lower binding affinity than the N-methyl analogue and so is less potent and not so widely used for this ...
... (Serentil) is a piperidine neuroleptic drug belonging to the class of drugs called phenothiazines, used in the treatment of schizophrenia. It is a metabolite of thioridazine. The drug's name is derived from the methylsulfoxy and piperidine functional groups in its chemical structure. It has central antiadrenergic, antidopaminergic, antiserotonergic and weak muscarinic anticholinergic effects. Serious side effects include akathisia, tardive dyskinesia and the potentially fatal neuroleptic malignant syndrome. Mesoridazine was withdrawn from the United States market in 2004 due to dangerous side effects, namely irregular heart beat and QT-prolongation of the electrocardiogram.[1] It currently appears to be unavailable worldwide. ...
... (C-(4,5,6-trimethoxyindan-1-yl)methanamine) is a conformationally-restricted derivative of the cactus-derived hallucinogen mescaline, which was discovered in 2006 by a team at Purdue University led by David E. Nichols. It acts as a potent agonist for the 5-HT2A and 5-HT2C receptors with the more active (R)-enantiomer having a Ki of 69 nM at the human 5-HT2A receptor, and around three times the potency of mescaline in drug-substitution experiments in animals.[1] This discovery that the side chain of the phenethylamine hallucinogens could be constrained to give chiral ligands with increased activity then led to the later development of the super-potent benzocyclobutene derivative TCB-2.[2][3] ...
Hallucinogenic Drug" means those specified in Section 7 of this rule including stramonium, mescaline or peyote, lysergic acid diethylamide, and psilocybin, and all synthetic equivalents of chemicals contained in resinous extractives of Cannabis sativa, or any salts or derivatives or compounds of any preparations or mixtures thereof, and any other substance having a hallucinogenic effect in the regulations adopted by the Board of Health under 18 V.S.A.§ 4202. ... • Cannabimimetic Agents means, collectively, any chemical that is a cannabinoid receptor type 1 (CB1) or cannabinoid receptor type 2 (CB2) agonist, or any salts, isomers, derivatives, or analogs of these chemicals. Structural classes include but are not limited to: (a) 2-(3-hydroxycyclohexyl)phenol with substitution at the 5-position of the phenolic ring by alkyl or alkenyl, whether or not substituted on the cyclohexyl ring to any extent. (b) 3-(1-naphthoyl)indole or 3-(1-naphthyl)indole with substitution at the nitrogen atom of the ...
... is a choline carbamate and a positively charged quaternary ammonium compound.[2] It is not well absorbed in the gastro-intestinal tract and does not cross the blood-brain barrier. It is usually administered topical ocular or through intraocular injection.[2] Carbachol is not easily metabolized by cholinesterase, it has a 2 to 5 minute onset of action and its duration of action is 4 to 8 hours with topical administration and 24 hours for intraocular administration. Since carbachol is poorly absorbed through topical administration, benzalkonium chloride is mixed in to promote absorption.[2]. Carbachol is a parasympathomimetic that stimulates both muscarinic and nicotinic receptors.[2] In topical ocular and intraocular administration its principal effects are miosis and increased aqueous humour outflow.[2]. In the cat and rat, carbachol is well known for its ability to induce rapid eye movement (REM) sleep when microinjected into the pontine reticular formation. Carbachol elicits this REM ...
... is widely used in preparations as an enhancing agent for some analgesics and antitussives (acetaminophen, dihydrocodeine, codeine, hydrocodone). It is widely used in certain parts of the world as cough suppressant usually with codeine, and sometimes by itself or in addition to dextromethorphan as it, like diphenhydramine, possesses antitussive action of its own and is particularly useful in semi-productive coughs because of its moderate drying action. Phenyltoloxamine has analgesic and anti-spasmodic properties of its own[citation needed] and is used in combination with paracetamol, aspirin and other salicylates and other drugs in proprietary preparations available over the counter for backache, muscle strains and similar conditions. In this respect, it is similar to a closely related antihistamine, orphenadrine, and both drugs are very closely related to diphenhydramine and to doxylamine, the latter of which is the active ingredient in NyQuil and many other cough ...
The effects of dissociatives can include sensory dissociation, hallucinations, mania, catalepsy, analgesia and amnesia.[5][6][7] The characteristic features of dissociative anesthesia were described as catalepsy, amnesia and analgesia.[5] According to Pender (1972), "the state has been designated as dissociative anesthesia since the patient truly seems disassociated from his environment."[8] Bonta (2004) described dissociative anaesthesia as "... a peculiar anaesthetic state in which marked sensory loss and analgesia as well as amnesia is not accompanied by actual loss of consciousness."[9] Both Pender (1970) and Johnstone et al. (1959) reported that patients under anaesthesia due to either ketamine or phencyclidine were prone to purposeless movements and had hallucinations (or "dreams"[10]) during and after anaesthesia. Some patients found the hallucinations euphoric while others found them disturbing. At sub-anesthetic doses, dissociatives alter many of the same cognitive and perceptual ...
Benactyzine has been used in the treatment of depression and is used in research to investigate the role of cholinergic systems ... Benactyzine. Subscribe to New Research on Benactyzine A centrally acting muscarinic antagonist. Benactyzine has been used in ... 02/01/1965 - "[BENACTYZINE POISONING IN A 3-YEAR-OLD BOY].". 02/01/2001 - "Benactyzine is used to treat organophosphate ... In contrast, benactyzine and trihexyphenidyl showed a third profile of activity: There was a smaller increase in drug dosage ...
The effect of the central cholinolytic benactyzine and the cholinomimetic arecoline on the uptake of45Ca by rat brain ... Semenov, E.V. Effect of benactyzine and arecoline on the45Ca uptake by rat brain nerve endings. Bull Exp Biol Med 86, 1168-1170 ... Effect of benactyzine and arecoline on the45Ca uptake by rat brain nerve endings. *E. V. Semenov ... Benactyzine was shown to depress the effect of arecoline and depolarization on uptake of the isotope. It is concluded that the ...
Benactyzine Hydrochloride. 10 mg. LGCFOR1826.00. In den Warenkorb Benaprizine Hydrochloride. 5 mg. LGCFOR1827.00. In den ...
Benactyzine has been used in the treatment of depression and is used in research to investigate the role of cholinergic systems ... Benactyzine Hydrochloride, also known as Suavitil, is a centrally acting muscarinic antagonist. ... Description: Benactyzine Hydrochloride, also known as Suavitil, is a centrally acting muscarinic antagonist. Benactyzine has ... Benactyzine Hydrochloride featured We are open as normal during COVID-19 pandemic. Order online, same day shipping out from ...
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Exfoliative dermatitis (ED) is a definitive term that refers to a scaling erythematous dermatitis involving 90% or more of the cutaneous surface. Exfoliative dermatitis is characterized by erythema and scaling involving the skins surface and often obscures the primary lesions that are important clues to understanding the evolution of the dis...
Antagonists: 3-Quinuclidinyl Benzilate • 4-DAMP • Atropine • Atropine Methonitrate • Benactyzine • Benzatropine (Benztropine ...
Benactyzine. Dibromotyrosine. Multivitamins Sirenitas - Neoterapici Benvegna Methimazole. Dibromotyrosine Bromazolo - Baldacci ...
Benactyzine. The therapeutic efficacy of Mineral oil can be decreased when used in combination with Benactyzine.. Withdrawn. ...
Benactyzine. The risk or severity of adverse effects can be increased when Tropicamide is combined with Benactyzine.. Withdrawn ...
Benactyzine (C20H25NO3). *Halazepam (C17H12ClF3N2O) ...
Benactyzine (C20H25NO3). *Chlorcyclizine (C18H21ClN2) ...
Bodur E, Cokuğraş AN, Tezcan EF (February 2001). "Inhibition effects of benactyzine and drofenine on human serum ...
Next Document: Efficacy of antidotal treatment against sarin poisoning: the superiority of benactyzine and caramiph.... ...
Benactyzine or its saltsPDL. I. DEC / 13. Benazepril or its salts or derivativesPDL. including but not limited to benazepril ...
Treatment for poisoning with GV involves drugs such as atropine, benactyzine, obidoxime, and HI-6. Fluorotabun ...
Benactyzine, Dicyclomine, N-Ethyl-3-piperidyl benzilate, N-Methyl-3-piperidyl benzilate, 3-Quinuclidinyl benzilate. ...
An exploratory study of the behavioral effects of Suavitil (benactyzine hydrochloride). Univ. Mich. Med. Bull., 1958, 24, 402- ...
Benactyzine hydrochloride Inhibitor 98.74% Benactyzine hydrochloride is a butyrylcholinesterase (BChE) inhibitor with a Ki of ...
... benactyzine-HCl. A dose-response relationship for vocalizations during the 30-sec trials was established, with 1 mg/kg being ...
Benactyzine; its salts; its quarternary compounds. Benapryzine; its salts. Bendrofluazide. Benethamine penicillin ...
... and Benactyzine being two examples. It is also used to determine zirconium and to get benzophenone. ...
3-Quinuclidinyl benzilate, WIN-2299, Salvinorin A, Mepyramine, Benactyzine Collection: Publisher: World Heritage Encyclopedia ...
BENACTYZINE 50500 BENDROFLUMETHIAZIDE 50502 BENOXAPROFEN 50505 BENOXINATE 50507 BENTIROMIDE 50508 BENTONITE 50511 BENZALDEHYDE ...
... diphenyl methane benactyzine), propanediol (mepropan) and trioxazin. ...
Benactyzine (substance). Code System Preferred Concept Name. Benactyzine (substance). Concept Status. Published. ...
Benactyzine hydrochloride (substance). Code System Preferred Concept Name. Benactyzine hydrochloride (substance). Concept ...
With the dye concentration of 2×10~(-3) mol/L, the mole ratio of dye-amine complex in the chloroform extract for benactyzine is ... The limits of detection of this dye for benethtropine [-1,1-diphenyl-2(3-tropanyl) ethane] and benactyzine (benzilic acid 2- ... The limits of detection of this dye for benethtropine [-1,1-diphenyl-2(3-tropanyl) ethane] and benactyzine (benzilic acid 2- ... and benactyzine(Ⅱ) are 16 ng/ml and 37 ng/ml respectively. The absorption coefficients (E_(1cm)~(1%) of these dye-amine ...
... benactyzine, benafentrine, benanserin, benapryzine, benaxibine, benazepril, bencianol, bencisteine, benclonidine, bencyclane, ...
InChI=1S/C26H37NO3/c1-18(2)26(29)30-25-13-12-21(17-28)16-24(25)23(22-10-8-7-9-11-22)14-15-27(19(3)4)20(5)6/h7-13,16,18-20,23,28H,14-15,17H2,1-6H3/t23-/m1/s1 ...

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