query: the only depolarizing muscle relaxant in clinical use is

pos: Neuromuscular-blocking drug after sufficient depolarization has occurred, phase II ("desensitizing phase") sets in and the muscle is no longer responsive to acetylcholine released by the motoneurons. At this point, full neuromuscular block has been achieved. The prototypical depolarizing blocking drug is succinylcholine (suxamethonium). It is the only such drug used clinically. It has a rapid onset (30 seconds) but very short duration of action (5–10 minutes) because of hydrolysis by various cholinesterases (such as butyrylcholinesterase in the blood). Succinylcholine was originally known as diacetylcholine because structurally it is composed of two acetylcholine molecules joined with a methyl group. Decamethonium is sometimes, but

pos: Muscle relaxant causing a depolarization of the end plate, resulting in muscle contraction. Following depolarization, the acetylcholine molecules are then removed from the end plate region and enzymatically hydrolysed by acetylcholinesterase. Normal end plate function can be blocked by two mechanisms. Nondepolarizing agents, such as tubocurarine, block the agonist, acetylcholine, from binding to nicotinic receptors and activating them, thereby preventing depolarization. Alternatively, depolarizing agents, such as succinylcholine, are nicotinic receptor agonists which mimic Ach, block muscle contraction by depolarizing to such an extent that it desensitizes the receptor and it can no longer initiate an action potential and cause muscle contraction. Both

pos: Neuromuscular-blocking drug blocking agent is a form of neuromuscular blocker that depolarizes the motor end plate. An example is succinylcholine. Depolarizing blocking agents work by depolarizing the plasma membrane of the muscle fiber, similar to acetylcholine. However, these agents are more resistant to degradation by acetylcholinesterase, the enzyme responsible for degrading acetylcholine, and can thus more persistently depolarize the muscle fibers. This differs from acetylcholine, which is rapidly degraded and only transiently depolarizes the muscle. There are two phases to the depolarizing block. During phase I ("depolarizing phase"), they cause muscular fasciculations (muscle twitches) while they are depolarizing the muscle fibers. Eventually,

pos: Assassination of Mahmoud Al-Mabhouh Dubai's police gave details of the death of al-Mabhouh after forensic tests. Al-Mabhouh was injected in his leg with succinylcholine, a quick-acting, depolarizing paralytic muscle relaxant. It causes almost-instant loss of motor skills, but does not induce loss of consciousness or anaesthesia. Then al-Mabhouh was suffocated. Al-Mazeina said, "The assassins used this method so that it would seem that his death was natural." Dubai's police chief, Lt. Gen. Dahi Khalfan Tamim, announced his preliminary conclusions on 18 February that, "Our investigations reveal that Mossad is involved in the murder of al-Mabhouh ... It is 99% if not 100% that Mossad

pos: Mivacurium chloride history of clinical anesthetic practice, the use of a "benzylisoquinoline" neuromuscular blocking agent. The heritage of mivacurium and indeed its very closely related cousin, doxacurium chloride, harks back to the synthesis of numerous compounds following structure-activity relationships that drove researchers to find the ideal replacement for succinylcholine (suxamethonium). Both mivacurium and doxacurium are descendants of early vigorous attempts to synthesize potent non-depolarizing agents with pharmacophores derived from cross-combinations of the non-depolarizing agent, laudexium, and the well-known depolarizing agent, succinylcholine (suxamethonium chloride). Ironically, laudexium itself was invented by a cross-combination between the prototypical non-depolarizing agent, d-tubocurarine and the depolarizing agent, decamethonium.

pos: Doxacurium chloride currently used neuromuscular blocking agents in this class because they are all, in fact, tetrahydroisoquinoline derivatives. By definition, therefore, there has never been, in the history of clinical anesthetic practice, the use of a "benzylisoquinoline" neuromuscular blocking agent. The heritages of doxacurium and mivacurium hark back to the synthesis of numerous compounds following structure-activity relationships that drove researchers to find the ideal replacement for succinylcholine (suxamethonium). Both doxacurium and mivacurium are descendants of early vigorous attempts to synthesize potent non-depolarizing agents with pharmacophoric elements derived from cross-combinations of the non-depolarizing agent, laudexium, and the well-known depolarizing agent, succinylcholine (suxamethonium). Ironically,

pos: Gantacurium chloride blocking drug has matched this feat to date: all other non-depolarizing neuromuscular blocking drugs clinically administered at equivalent doses most certainly would result in a medium or long duration of action albeit with a rapid onset of paralyzing effect. In this sense, gantacurium is a first in its class non-depolarizing neuromuscular blocking drug to arguably challenge the pharmacological profile of the gold-standard ultrashort acting depolarizing agent succinylcholine (suxamethonium). BW785U77 was not pursued for further clinical development owing to its propensity for eliciting histamine release in humans with more intensity than that observed during pre-clinical evaluation in animals. The holy grail

pos: Electroconvulsive therapy the seizure resulted in a full-scale convulsion. A rare but serious complication of unmodified ECT was fracture or dislocation of the long bones. In the 1940s, psychiatrists began to experiment with curare, the muscle-paralysing South American poison, in order to modify the convulsions. The introduction of suxamethonium (succinylcholine), a safer synthetic alternative to curare, in 1951 led to the more widespread use of "modified" ECT. A short-acting anesthetic was usually given in addition to the muscle relaxant in order to spare patients the terrifying feeling of suffocation that can be experienced with muscle relaxants. The steady growth of antidepressant use

pos: History of electroconvulsive therapy in the United States why ECT has been recommended for them, the treatment process initially and throughout the course, allaying fears of the patient or their family may have about ECT and directing their attention to scientific fact and evidence supporting its use” The client is then given a short-acting anesthetic, such as methohexital, and also given a muscle relaxant, such as succinylcholine. Once the determination of muscle paralysis is determined, a mild electrical current is administered to the patient’s brain. Paralysis is determined by observing the extremity that the blood pressure cuff is placed on. The blood pressure is inflated to stop the

pos: History of electroconvulsive therapy in the United Kingdom succinylcholine, a safer synthetic alternative to curare, led to the more widespread use of modified ECT. A short-acting anaesthetic was usually given in addition to the muscle relaxant in order to spare patients the terrifying feeling of suffocation that can be experienced with muscle relaxants. By the mid 1950s most hospitals in Britain routinely used modified ECT, although a few still used unmodified ECT or ECT with muscle relaxants but without anaesthetic. In 1957 a patient who had sustained fractures to both hips whilst undergoing unmodified ECT at a London hospital took legal action. He lost the case but it

neg: Gantacurium chloride Gantacurium chloride Gantacurium chloride (formerly recognized as GW280430A and as AV430A) is a new experimental neuromuscular blocking drug or skeletal muscle relaxant in the category of non-depolarizing neuromuscular-blocking drugs, used adjunctively in surgical anesthesia to facilitate endotracheal intubation and to provide skeletal muscle relaxation during surgery or mechanical ventilation. Gantacurium is not yet available for widespread clinical use: it is currently undergoing Phase III clinical development. Gantacurium represents the third generation of tetrahydroisoquinolinium (THIQ) neuromuscular blocking drugs in a long lineage of compounds invented by medicinal chemists and scientists at Burroughs Wellcome Co., Research Triangle Park, North Carolina. Unlike all

neg: Laudexium metilsulfate antagonized by anticholinesterases. The displacement of laudexium from clinical use was assured owing to recurrent reports of significant post-operative re-curarization. Laudexium metilsulfate Laudexium metilsulfate is a neuromuscular blocking drug or skeletal muscle relaxant in the category of non-depolarizing neuromuscular-blocking drugs, used adjunctively in surgical anesthesia to facilitate endotracheal intubation and to provide skeletal muscle relaxation during surgery or mechanical ventilation. Laudexium is no longer used in clinical practice, though it was introduced clinically in the early 1950s. It has about half the potency, a slower onset of action and a duration of action much longer than that of "d"-tubocurarine. As

neg: Laudexium metilsulfate Laudexium metilsulfate Laudexium metilsulfate is a neuromuscular blocking drug or skeletal muscle relaxant in the category of non-depolarizing neuromuscular-blocking drugs, used adjunctively in surgical anesthesia to facilitate endotracheal intubation and to provide skeletal muscle relaxation during surgery or mechanical ventilation. Laudexium is no longer used in clinical practice, though it was introduced clinically in the early 1950s. It has about half the potency, a slower onset of action and a duration of action much longer than that of "d"-tubocurarine. As with all clinically established (as well as experimental agents) with a non-depolarizing mechanism of action, its pharmacological action can be

neg: Gantacurium chloride and these two agents (cisatracurium and atracurium)—in particular, the reverse positioning of the carboxyl ester and onium nitrogen groups—absolutely ensures that gantacurium will never undergo Hofmann elimination just as is the case with mivacurium and doxacurium. Gantacurium chloride Gantacurium chloride (formerly recognized as GW280430A and as AV430A) is a new experimental neuromuscular blocking drug or skeletal muscle relaxant in the category of non-depolarizing neuromuscular-blocking drugs, used adjunctively in surgical anesthesia to facilitate endotracheal intubation and to provide skeletal muscle relaxation during surgery or mechanical ventilation. Gantacurium is not yet available for widespread clinical use: it is currently undergoing Phase III

neg: Candocuronium iodide Candocuronium iodide Candocuronium iodide (INN, formerly chandonium, HS-310) is an aminosteroid neuromuscular-blocking drug or skeletal muscle relaxant in the category of non-depolarizing neuromuscular-blocking drugs. Its potential adjunctive use in anesthesia to facilitate endotracheal intubation and to provide skeletal muscle relaxation during surgery or mechanical ventilation was briefly evaluated in clinical studies in India, but further development discontinued because of attendant cardiovasular effects, primarily tachycardia that was no worse than but also not an improvement over the clinically established pancuronium bromide. Candocuronium demonstrated a short duration and a rapid onset of action, with little or no ganglion blocking activity, and it

neg: BW-A444 BW-A444 BW A444U was an experimental neuromuscular blocking drug or skeletal muscle relaxant in the category of non-depolarizing neuromuscular-blocking drugs, intended to be used adjunctively in surgical anesthesia to facilitate endotracheal intubation and to provide skeletal muscle relaxation during surgery or mechanical ventilation. It was synthesized and developed in the early 1980s. BW A444U represented the first-generation of tetrahydroisoquinoline neuromuscular-blocking drugs that are nicotinic acetylcholine receptor antagonists or antinicotinics. It was an intermediate-duration non-depolarizing neuromuscular-blocking drug or skeletal muscle relaxant. It was synthesized by Mary M. Jackson and James C. Wisowaty, PhD (both chemists within the Chemical Development Laboratories at

neg: Pancuronium bromide Pancuronium bromide Pancuronium (trademarked as Pavulon) is an aminosteroid muscle relaxant with various medical uses. It is used in euthanasia and is the second of three drugs administered during most lethal injections in the United States. Pancuronium is a typical non-depolarizing curare-mimetic muscle relaxant. It competitively inhibits the nicotinic acetylcholine receptor at the neuromuscular junction by blocking the binding of acetylcholine. It has slight vagolytic activity, causing an increase in heart rate, but no ganglioplegic (i.e., blocking ganglions) activity. It is a very potent muscle relaxant drug, with an ED95 (i.e., the dose that causes 95% depression of muscle twitch

neg: Candocuronium iodide testing. The discovery of candocuronium led to numerous related neuromuscular blocking agents with short durations of action but also having attendant undesirable cardiovascular effects. The Marshall group then explored other modifications at the 3- and 16-positions of the androstane nucleus, but the work has not yet yielded an agent worthy of expanded evaluation to clinical testing in this azasteroidal class of neuromuscular blocking agents. Candocuronium iodide Candocuronium iodide (INN, formerly chandonium, HS-310) is an aminosteroid neuromuscular-blocking drug or skeletal muscle relaxant in the category of non-depolarizing neuromuscular-blocking drugs. Its potential adjunctive use in anesthesia to facilitate endotracheal intubation and to

neg: Voluntary euthanasia the most reliable and rapid way to accomplish euthanasia. A coma is first induced by intravenous administration of 20 mg/kg sodium thiopental (Nesdonal) in a small volume (10 ml physiological saline). Then a triple intravenous dose of a non-depolarizing neuromuscular muscle relaxant is given, such as 20 mg pancuronium bromide (Pavulon) or 20 mg vecuronium bromide (Norcuron). The muscle relaxant should preferably be given intravenously, in order to ensure optimal availability. Only for pancuronium bromide (Pavulon) are there substantial indications that the agent may also be given intramuscularly in a dosage of 40 mg. With regards to voluntary euthanasia, many

neg: BW-A444 Burroughs Wellcome Co., Research Triangle Park, NC) in collaboration with John J. Savarese MD (who at the time was an anesthesiologist in the Dept. of Anesthesia, Harvard Medical School at the Massachusetts General Hospital, Boston, MA). The drug was tested clinically in the early 1980s, and quickly abandoned from further clinical development after a single clinical study, owing primarily to undesirable effects of histamine release when administered at clinically relevant doses. BW-A444 BW A444U was an experimental neuromuscular blocking drug or skeletal muscle relaxant in the category of non-depolarizing neuromuscular-blocking drugs, intended to be used adjunctively in surgical anesthesia to

neg: Mivacurium chloride ester moiety. The second ester is metabolized much more slowly, although the lack of a bis-quaternary structure effectively terminates the neuromusuclar blocking action. Mivacurium chloride Mivacurium chloride (formerly recognized as BW1090U81, BW B1090U or BW1090U) is a short-duration non-depolarizing neuromuscular-blocking drug or skeletal muscle relaxant in the category of non-depolarizing neuromuscular-blocking drugs, used adjunctively in anesthesia to facilitate endotracheal intubation and to provide skeletal muscle relaxation during surgery or mechanical ventilation. Mivacurium is a symmetrical molecule although it is a mixture of three of the twenty possible isomers: the isomerism stems from chirality at the C-1 carbon position of both

neg: Mivacurium chloride Mivacurium chloride Mivacurium chloride (formerly recognized as BW1090U81, BW B1090U or BW1090U) is a short-duration non-depolarizing neuromuscular-blocking drug or skeletal muscle relaxant in the category of non-depolarizing neuromuscular-blocking drugs, used adjunctively in anesthesia to facilitate endotracheal intubation and to provide skeletal muscle relaxation during surgery or mechanical ventilation. Mivacurium is a symmetrical molecule although it is a mixture of three of the twenty possible isomers: the isomerism stems from chirality at the C-1 carbon position of both the tetrahydroisoquinolinium rings, as well as both the positively charged nitrogen (onium) heads, and the E/Z diastereomerism at the C=C double bond of

neg: Pancuronium bromide It was also used by the Skin Hunters to kill patients in the Polish city of Łódź. Pavulon was also used by Richard Angelo in 1987 to kill at least 10 patients under his care at the Good Samaritan Hospital in New York. Pancuronium bromide Pancuronium (trademarked as Pavulon) is an aminosteroid muscle relaxant with various medical uses. It is used in euthanasia and is the second of three drugs administered during most lethal injections in the United States. Pancuronium is a typical non-depolarizing curare-mimetic muscle relaxant. It competitively inhibits the nicotinic acetylcholine receptor at the neuromuscular junction by blocking

neg: Doxacurium chloride Doxacurium chloride Doxacurium chloride (formerly recognized as BW938U80 or BW A938U) is a neuromuscular-blocking drug or skeletal muscle relaxant in the category of non-depolarizing neuromuscular-blocking drugs, used adjunctively in anesthesia to provide skeletal muscle relaxation during surgery or mechanical ventilation. Unlike a number of other related skeletal muscle relaxants, it is rarely used adjunctively to facilitate endotracheal intubation. Doxacurium is a symmetrical molecule because it is a diester of succinic acid. The pharmacological action of doxacurium is a function of its competitive antagonism to acetylcholine receptors of the nicotinic type. The drug is marketed worldwide under the tradename of Nuromax,

neg: Decamethonium acetylcholine release. Decamethonium does not produce unconsciousness or anesthesia, and its effects may cause considerable psychological distress while simultaneously making it impossible for a patient to communicate. For these reasons, administration of the drug to a conscious patient is strongly advised against, except in necessary emergency situations. Decamethonium was used clinically in the UK for many years, but it is now available only for research purposes. Decamethonium Decamethonium (Syncurine) is a depolarizing muscle relaxant or neuromuscular blocking agent, and is used in anesthesia to induce paralysis. Decamethonium, which has a short action time, is similar to acetylcholine and acts as

neg: Neuromuscular-blocking drug Most of the agents in this category would be classified as non-depolarizing. Gallamine is a trisquaternary ether with three ethonium heads attached to a phenyl ring through an ether linkage. Many other different structures have been used for their muscle relaxant effect such as alcuronium (alloferin), anatruxonium, diadonium, fazadinium (AH8165) and tropeinium. In recent years much research has been devoted to new types of quaternary ammonium muscle relaxants. These are asymmetrical diester isoquinolinium compounds and bis-benzyltropinium compounds that are bistropinium salts of various diacids. These classes have been developed to create muscle relaxants that are faster and shorter acting. Both

neg: Nectandra tannins play important roles as antioxidant compounds in the scavenging of free radicals. It is reported that an extract of "N. salicifolia" has potent relaxant activity on vascular smooth muscle. Researchers of the entire world agree that pre-clinical large studies on herbal medicine are important and urgent, specially high-quality clinical and pre-clinical trials. In pre-Columbian Peru the seeds, called "Amala" in Spanish, were used as a muscle relaxant. In sites of the Sican culture, collections of the seeds have been associated with human sacrifice, and used to incapcitate victims prior to being killed. "Nectandra" contains the following species (but this

neg: Decamethonium Decamethonium Decamethonium (Syncurine) is a depolarizing muscle relaxant or neuromuscular blocking agent, and is used in anesthesia to induce paralysis. Decamethonium, which has a short action time, is similar to acetylcholine and acts as a partial agonist of the nicotinic acetylcholine receptor. In the motor endplate, it causes depolarization, preventing further effects to the normal release of acetylcholine from the presynaptic terminal, and therefore preventing the neural stimulus from affecting the muscle. In the process of binding, decamethonium activates (depolarizes) the motor endplate - but since the decamethonium itself is not degraded, the membrane remains depolarized and unresponsive to normal

neg: Rocuronium bromide Rocuronium bromide Rocuronium bromide (brand names Zemuron, Esmeron) is an aminosteroid non-depolarizing neuromuscular blocker or muscle relaxant used in modern anaesthesia to facilitate tracheal intubation by providing skeletal muscle relaxation, most commonly required for surgery or mechanical ventilation. It is used for standard endotracheal intubation, as well as for rapid sequence induction (RSI) where suxamethonium chloride, the preferred drug for RSI, is contraindicated or unavailable. It was designed to be a weaker antagonist at the neuromuscular junction than pancuronium; hence its monoquaternary structure and its having an allyl group and a pyrrolidine group attached to the D ring quaternary nitrogen

neg: Rocuronium bromide lethal injection, with rocuronium bromide. On 3 October 2016, the U.S. state of Ohio announced that it would resume executions on January 12, 2017, using a combination of midazolam, rocuronium bromide, and potassium chloride. Prior to this, the last execution in Ohio was in January 2014. On August 24, 2017, the U.S. state of Florida executed Mark James Asay using a combination of etomidate, rocuronium bromide, and potassium acetate. Rocuronium bromide Rocuronium bromide (brand names Zemuron, Esmeron) is an aminosteroid non-depolarizing neuromuscular blocker or muscle relaxant used in modern anaesthesia to facilitate tracheal intubation by providing skeletal muscle relaxation, most

neg: Cisatracurium besilate (4). Alkylation with methyl benzenesulfonate forms the bis-quaternary salt, affording cisatracuronium (5). Cisatracurium besilate Cisatracurium besilate (INN; cisatracurium besylate (USAN); formerly recognized as 51W89; trade name Nimbex) is a bisbenzyltetrahydroisoquinolinium that has effect as a neuromuscular-blocking drug or skeletal muscle relaxant in the category of non-depolarizing neuromuscular-blocking drugs, used adjunctively in anesthesia to facilitate endotracheal intubation and to provide skeletal muscle relaxation during surgery or mechanical ventilation. It shows intermediate duration of action. Cisatracurium is one of the ten isomers of the parent molecule, atracurium. Moreover, cisatracurium represents approximately 15% of the atracurium mixture. The generic name cisatracurium was conceived

neg: Cisatracurium besilate Cisatracurium besilate Cisatracurium besilate (INN; cisatracurium besylate (USAN); formerly recognized as 51W89; trade name Nimbex) is a bisbenzyltetrahydroisoquinolinium that has effect as a neuromuscular-blocking drug or skeletal muscle relaxant in the category of non-depolarizing neuromuscular-blocking drugs, used adjunctively in anesthesia to facilitate endotracheal intubation and to provide skeletal muscle relaxation during surgery or mechanical ventilation. It shows intermediate duration of action. Cisatracurium is one of the ten isomers of the parent molecule, atracurium. Moreover, cisatracurium represents approximately 15% of the atracurium mixture. The generic name cisatracurium was conceived by scientists at Burroughs Wellcome Co. (now part of GlaxoSmithKline) by combining

neg: Muscle relaxant at the level of the cortex, brain stem or spinal cord, or all three areas, they have traditionally been referred to as "centrally acting" muscle relaxants. However, it is now known not every agent in this class has CNS activity (e.g. dantrolene), so this name is inaccurate. Most sources still use the term "centrally acting muscle relaxant". According to MeSH, dantrolene is usually classified as a centrally acting muscle relaxant. The World Health Organization, in its ATC, uses the term "centrally acting agents", but adds a distinct category of "directly acting agents", for dantrolene. Use of this terminology dates back

neg: Muscle relaxant pain and spasms and to reduce spasticity in a variety of neurological conditions. While both neuromuscular blockers and spasmolytics are often grouped together as muscle relaxants, the term is commonly used to refer to spasmolytics only. The earliest known use of muscle relaxant drugs was by natives of the Amazon Basin in South America who used poison-tipped arrows that produced death by skeletal muscle paralysis. This was first documented in the 16th century, when European explorers encountered it. This poison, known today as curare, led to some of the earliest scientific studies in pharmacology. Its active ingredient, tubocurarine, as well

neg: Mephenesin Mephenesin Mephenesin is a centrally acting muscle relaxant. It can be used as an antidote for strychnine poisoning. Mephenesin however presents with the major drawbacks of having a short duration of action and a much greater effect on the spinal cord than the brain, resulting in pronounced respiratory depression at clinical doses and therefore a very low therapeutic index. It is especially dangerous and potentially fatal in combination with alcohol and other depressants. Mephenesin was used by Bernard Ludwig and Frank Berger to synthesize meprobamate, the first tranquilizer to see widespread clinical use. Mephenesin is no longer available in North

neg: Sodium thiopental agent to induce coma, followed by pancuronium bromide to paralyze muscles and stop breathing. Intravenous administration is the most reliable and rapid way to accomplish euthanasia. Death is quick. A coma is first induced by intravenous administration of 20 mg/kg thiopental sodium (Nesdonal) in a small volume (10 ml physiological saline). Then, a triple dose of a non-depolarizing neuromuscular blocking drug is given, such as 20 mg pancuronium bromide (Pavulon) or 20 mg vecuronium bromide (Norcuron). The muscle relaxant should be given intravenously to ensure optimal availability but pancuronium bromide may be administered intramuscularly at an increased dosage level of

neg: Curare skeletal muscles, effectively paralyzing the muscles of the body. Since tubocurarine binds reversibly to the ACh receptors, treatment for curare poisoning involves adding an acetylcholinesterase (AChE) inhibitor, which will stop the destruction of acetylcholine so that it can compete with curare. Curare is an example of a non-depolarizing muscle relaxant that blocks the nicotinic acetylcholine receptor (nAChR), one of the two types of acetylcholine (ACh) receptors, at the neuromuscular junction. The main toxin of curare, d-tubocurarine, occupies the same position on the receptor as ACh with an equal or greater affinity, and elicits no response, making it a competitive antagonist.

neg: Suxamethonium chloride ventilation is not maintained. Normal treatment is to maintain sedation and ventilate the patient on an intensive care unit until muscle function has returned. Blood testing for cholinesterase function can be performed. Mivacurium, a non-depolarizing neuromuscular blocking drug, is also metabolized via the same route with a similar clinical effect in patients deficient in plasma cholinesterase activity. Deliberate induction of conscious apnea using this drug led to its use as a form of aversion therapy in the 1960s and 1970s in some prison and institutional settings. This use was discontinued after negative publicity concerning the terrifying effects on subjects of

neg: Muscle relaxant Muscle relaxant A muscle relaxant is a drug that affects skeletal muscle function and decreases the muscle tone. It may be used to alleviate symptoms such as muscle spasms, pain, and hyperreflexia. The term "muscle relaxant" is used to refer to two major therapeutic groups: neuromuscular blockers and spasmolytics. Neuromuscular blockers act by interfering with transmission at the neuromuscular end plate and have no central nervous system (CNS) activity. They are often used during surgical procedures and in intensive care and emergency medicine to cause temporary paralysis. Spasmolytics, also known as "centrally acting" muscle relaxants, are used to alleviate musculoskeletal

neg: Fabomotizole has found little clinical use outside Russia and has not been evaluated by the FDA. Fabomotizole Fabomotizole (INN) (brand name Afobazole) is an anxiolytic drug launched in Russia in the early 2000s. It produces anxiolytic and neuroprotective effects without any sedative or muscle relaxant actions. Its mechanism of action remains poorly defined however, with GABAergic, NGF- and BDNF-release-promoting, MT1 receptor agonism, MT3 receptor antagonism, and sigma agonism suggested as potential mechanisms. Fabomotizole was shown to inhibit MAO-A reversibly and there might be also some involvement with serotonin receptors. Clinical trials have shown fabomotizole to be well tolerated and reasonably effective

neg: Ammi visnaga the kidneys and acts as a diuretic. Its clinical effects in humans are unknown. Khellin, a chemical compound obtained from "A. visnaga", was used at one time as a smooth muscle relaxant, but its use is limited due to adverse side effects. Amiodarone and cromoglycate are synthetic derivatives of khellin with fewer side effects which were developed for use in modern medicine. Visnagin is another chemical compound which is found in "A. visnaga". Visnadine is a natural vasodilator found in "A. visnaga" Ammi visnaga Ammi visnaga is a species of flowering plant in the carrot family known by many common

neg: Atracurium besilate John B. Stenlake's medicinal chemistry research group in the Department of Pharmacy at Strathclyde University, Scotland. Dewar first named this compound "33A74" before its eventual emergence in the clinic as atracurium. Atracurium was the culmination of a rational approach to drug design to produce the first non-depolarizing non-steroidal skeletal muscle relaxant that undergoes chemodegradation "in vivo". The term chemodegradation was coined by Roger D. Waigh, Ph.D., also a pharmacist and a postdoctoral researcher in Stenlake's research group. Atracurium was licensed by Strathclyde University to the Wellcome Foundation UK, which developed the drug (then known as BW 33A) and its introduction

neg: Biological functions of hydrogen sulfide hydrogen sulfide induced hypothermia "in humans" had completed Phase I clinical trials. The clinical trials commissioned by the company he helped found, Ikaria, were however withdrawn or terminated by August 2011. Biological functions of hydrogen sulfide Hydrogen sulfide is produced in small amounts by some cells of the mammalian body and has a number of biological signaling functions. (Only two other such gases are currently known: nitric oxide (NO) and carbon monoxide (CO).) The gas is produced from cysteine by the enzymes cystathionine beta-synthase and cystathionine gamma-lyase. It acts as a relaxant of smooth muscle and as a vasodilator and

neg: Muscle relaxant shown to be better than another, and all of them have adverse effects, particularly dizziness and drowsiness. Concerns about possible abuse and interaction with other drugs, especially if increased sedation is a risk, further limit their use. A muscle relaxant is chosen based on its adverse-effect profile, tolerability, and cost. Muscle relaxants (according to one study) were not advised for orthopedic conditions, but rather for neurological conditions such as spasticity in cerebral palsy and multiple sclerosis. Dantrolene, although thought of primarily as a peripherally acting agent, is associated with CNS effects, whereas baclofen activity is strictly associated with the CNS.

neg: Mephenesin America but is used in France, Italy and a few other countries. Its use has largely been replaced by the related drug methocarbamol, which is better absorbed. Mephenesin may be an NMDA receptor antagonist. Mephenesin Mephenesin is a centrally acting muscle relaxant. It can be used as an antidote for strychnine poisoning. Mephenesin however presents with the major drawbacks of having a short duration of action and a much greater effect on the spinal cord than the brain, resulting in pronounced respiratory depression at clinical doses and therefore a very low therapeutic index. It is especially dangerous and potentially fatal

neg: Anxiolytic been replaced with benzodiazepines while the drug is now withdrawn in many European countries and Canada. The muscle relaxant carisoprodol has anxiolytic effects by metabolizing to meprobamate. Various other carbamates have been found to share these effects, such as tybamate and lorbamate. Hydroxyzine (Atarax) is an antihistamine originally approved for clinical use by the FDA in 1956. In addition to its antihistamine properties hydroxyzine possesses anxiolytic properties and is approved for the treatment of anxiety and tension. Its sedative properties are useful as a premedication before anesthesia or to induce sedation after anesthesia. Hydroxyzine has been shown to be as

neg: Muscle relaxant compounds have also been shown to reduce muscle spasms by their central nervous system activity. Tizanidine is perhaps the most thoroughly studied clonidine analog, and is an agonist at α-adrenergic receptors, but reduces spasticity at doses that result in significantly less hypotension than clonidine. Neurophysiologic studies show that it depresses excitatory feedback from muscles that would normally increase muscle tone, therefore minimizing spasticity. Furthermore, several clinical trials indicate that tizanidine has a similar efficacy to other spasmolytic agents, such as diazepam and baclofen, with a different spectrum of adverse effects. The hydantoin derivative dantrolene is a spasmolytic agent with a

neg: Muscle relaxant difficulty breathing, tightness in the chest, swelling of the mouth, face, lips, or tongue), chills, fever, and sore throat, may require medical attention. Other severe side effects include unusual or severe tiredness or weakness, as well as yellowing of the skin or the eyes. When baclofen is administered intrathecally, it may cause CNS depression accompanied with cardiovascular collapse and respiratory failure. Tizanidine may lower blood pressure. This effect can be controlled by administering a low dose at the beginning and increasing it gradually. Muscle relaxant A muscle relaxant is a drug that affects skeletal muscle function and decreases the muscle

neg: Malignant hyperthermia rapidly on clinical suspicion of the onset of malignant hyperthermia. Dantrolene is a muscle relaxant that appears to work directly on the ryanodine receptor to prevent the release of calcium. After the widespread introduction of treatment with dantrolene, the mortality of malignant hyperthermia fell from 80% in the 1960s to less than 5%. Dantrolene remains the only drug known to be effective in the treatment of MH. The recommended dose of dantrolene is 2.5 mg/kg, repeated as necessary. It is recommended that each hospital keeps a minimum stock of 36 dantrolene vials (720 mg), sufficient for four doses in a

neg: Deramciclane inhibitor of CYP2D6. Some studies also show the drug to have moderate affinity to dopamine D2 receptors and low affinity to dopamine receptor D1. Researchers are looking for alternatives to benzodiazepines for anxiolytic use because benzodiazepine drugs have sedative and muscle relaxant side effects. Deramciclane was discovered by EGIS Pharmaceuticals Ltd in Budapest, Hungary. In 2000, EGIS signed over exclusive rights to Orion Pharma to further develop, register, and market deramciclane. Successful pre-clinical, Phase I, and Phase II trials looked promising to the company and its investors even up until the third quarter of 2002. Phase I studies show little

neg: Tolperisone 12 hours. Tolperisone Tolperisone, a piperidine derivative, is a centrally acting muscle relaxant. Trade names include Biocalm, Muscodol, Mydeton, Mydocalm, Mydoflex, Myolax, Myoxan and Viveo. Tolperisone is indicated for use in the treatment of pathologically increased tone of the cross-striated muscle caused by neurological diseases (damage of the pyramidal tract, multiple sclerosis, myelopathy, encephalomyelitis) and of spastic paralysis and other encephalopathies manifested with muscular dystonia. Other possible uses include: Manufacturers report that tolperisone should not be used in patients with myasthenia gravis. Only limited data are available regarding the safety in children, youths, during pregnancy and breastfeeding. It is not

neg: Tolperisone Tolperisone Tolperisone, a piperidine derivative, is a centrally acting muscle relaxant. Trade names include Biocalm, Muscodol, Mydeton, Mydocalm, Mydoflex, Myolax, Myoxan and Viveo. Tolperisone is indicated for use in the treatment of pathologically increased tone of the cross-striated muscle caused by neurological diseases (damage of the pyramidal tract, multiple sclerosis, myelopathy, encephalomyelitis) and of spastic paralysis and other encephalopathies manifested with muscular dystonia. Other possible uses include: Manufacturers report that tolperisone should not be used in patients with myasthenia gravis. Only limited data are available regarding the safety in children, youths, during pregnancy and breastfeeding. It is not known whether

neg: Sugammadex approved for use in the European Union on July 29, 2008. Sugammadex Sugammadex (Org 25969, tradename Bridion) is an agent for reversal of neuromuscular blockade by the agent rocuronium in general anaesthesia. It is the first selective relaxant binding agent (SRBA). Sugammadex is used to reverse neuromuscular blockade after administration of non-depolarizing neuromuscular-blocking agents such as vecuronium or rocuronium. Sugammadex is a modified γ-cyclodextrin, with a lipophilic core and a hydrophilic periphery. This gamma cyclodextrin has been modified from its natural state by placing eight carboxyl thio ether groups at the sixth carbon positions. These extensions extend the cavity size

neg: Pasteur Institute or the first synthetic no-depolarising muscle relaxant (Flaxedil). The discovery of the therapeutic properties of sulfanilamide by Tréfouël, Nitti and Bovet, in the laboratory of Fourneau, paved the way for the sulfamidotherapy. The Hospital Pasteur was built during the first years of the 20th century in front of the Institute, and was employed for a long time by the members as a field for clinical observation and experimentations of therapeutical processes elaborated by themselves. Since in the beginning it was provided with only 120 beds, every patient was so well isolated in his private room that each room could be

neg: Prostaglandin EP4 receptor various diseases including ulcerative colitis, Alzheimer's disease, osteoporosis, and certain cardiovascular diseases. Inhibitory receptor antagonists for EP, including grapiprant (CJ-023,423), ONO-AE3-208, GW627368X, AH23848, and ONO-AE2-227, are in development for possible clinical us as inhibitors of the progression of prostate, breast, colon, and lung cancers. EP is classified as a relaxant type of prostaglandin receptor based on its ability, upon activation, to relax the contraction of certain smooth muscle preparations and smooth muscle-containing tissues that have been pre-contracted by stimulation. When bound to PGE or other of its agonists, it mobilizes G proteins containing the Gs alpha subunit (i.e. Gα)-G beta-gammaes

neg: Methocarbamol Methocarbamol Methocarbamol is a central muscle relaxant used to treat skeletal muscle spasms. Under the trade name Robaxin, it is marketed by Actient Pharmaceuticals in the United States and Pfizer in Canada. The mechanism of action of methocarbamol is currently unknown, but may involve the inhibition of carbonic anhydrase. The muscle relaxant effects of methocarbamol are largely attributed to central depressant effects; however, peripheral effects of methocarbamol to prolong muscle refractory period have also been reported. Potential side-effects include: drowsiness, dizziness, clumsiness (ataxia), upset stomach, flushing, blurred vision, and fever. Both tachycardia (fast heart rate) and bradycardia (slow heart rate)

neg: Muscle relaxant unique mechanism of action outside of the CNS. It reduces skeletal muscle strength by inhibiting the excitation-contraction coupling in the muscle fiber. In normal muscle contraction, calcium is released from the sarcoplasmic reticulum through the ryanodine receptor channel, which causes the tension-generating interaction of actin and myosin. Dantrolene interferes with the release of calcium by binding to the ryanodine receptor and blocking the endogenous ligand ryanodine by competitive inhibition. Muscle that contracts more rapidly is more sensitive to dantrolene than muscle that contracts slowly, although cardiac muscle and smooth muscle are depressed only slightly, most likely because the release of

neg: Chlorphenesin carbamate Chlorphenesin carbamate Chlorphenesin carbamate (Maolate, Musil) is a centrally acting muscle relaxant used to treat muscle pain and spasms. Chlorphenesin is no longer used for this purpose in most developed nations due to the availability of much safer spasmolytics such as benzodiazepines. Other central effects include sedation, anxiolysis, and dizziness. It also has antifungal and some antibacterial properties and is thus classified as an antifungal for topical use by the WHO. The major adverse effect from this preservative on skin is allergic contact sensitivity. Systemic intoxication from transdermal use has not been observed, although the FDA discourages its use as

neg: Vasomotion coupling is present between the vascular smooth muscle cells, the endothelial cells and the endothelial to vascular smooth muscle cells. An initial depolarizing current leads to the opening of the voltage-dependent calcium channels, ultimately resulting in synchronization of individual calcium levels. When patch clamp recordings are conducted, depolarization occurs in the endothlial layer at the same time as the underlying vascular smooth muscle. The cause of the initial depolarizing current, however, remains to be determined. Mathematical modeling has pointed to the existence of 2-4 independent non-linear oscillating systems interacting to produce vasomotion. It is possible that in order for vasomotion

neg: Muscle relaxant Muscle relaxants are thought to be useful in painful disorders based on the theory that pain induces spasm and spasm causes pain. However, considerable evidence contradicts this theory. In general, muscle relaxants are not approved by FDA for long-term use. However, rheumatologists often prescribe cyclobenzaprine nightly on a daily basis to increase stage 4 sleep. By increasing this sleep stage, patients feel more refreshed in the morning. Improving sleep is also beneficial for patients who have fibromyalgia. Muscle relaxants such as tizanidine are prescribed in the treatment of tension headaches. Diazepam and carisoprodol are not recommended for older adults, pregnant

neg: Methocarbamol as Robaxisal in the U.S. and Canada. However, in Spain the tradename Robaxisal is used for the Paracetamol combination instead of Robaxacet. These combinations are also available from independent manufacturers under generic names. Methocarbamol Methocarbamol is a central muscle relaxant used to treat skeletal muscle spasms. Under the trade name Robaxin, it is marketed by Actient Pharmaceuticals in the United States and Pfizer in Canada. The mechanism of action of methocarbamol is currently unknown, but may involve the inhibition of carbonic anhydrase. The muscle relaxant effects of methocarbamol are largely attributed to central depressant effects; however, peripheral effects of methocarbamol

neg: Neuromuscular-blocking drug of the two α-subunits of the receptor. Each receptive site has two subsites, an anionic site that binds to the cationic ammonium head and a site that binds to the blocking agent by donating a hydrogen bond. Non-depolarizing agents A decrease in binding of acetylcholine leads to a decrease in its effect and neuron transmission to the muscle is less likely to occur. It is generally accepted that non-depolarizing agents block by acting as reversible competitive inhibitors. That is, they bind to the receptor as antagonists and that leaves fewer receptors available for acetylcholine to bind. Depolarizing agents Depolarizing agents

neg: Muscle relaxant dantrolene, baclofen, Drugs once but no longer or very rarely used to relax skeletal muscles include meprobamate, barbiturates, methaqualone, glutethimide and the like; some subcategories of opioids have muscle relaxant properties, and some are marketed in combination drugs with skeletal and/or smooth muscle relaxants such as whole opium products, some ketobemidone, piritramide and fentanyl preparations and Equagesic. Muscle relaxation and paralysis can theoretically occur by interrupting function at several sites, including the central nervous system, myelinated somatic nerves, unmyelinated motor nerve terminals, nicotinic acetylcholine receptors, the motor end plate, and the muscle membrane or contractile apparatus. Most neuromuscular blockers function

neg: Chlorphenesin carbamate an ingredient in nipple cream for nursing mothers. Chlorphenesin carbamate Chlorphenesin carbamate (Maolate, Musil) is a centrally acting muscle relaxant used to treat muscle pain and spasms. Chlorphenesin is no longer used for this purpose in most developed nations due to the availability of much safer spasmolytics such as benzodiazepines. Other central effects include sedation, anxiolysis, and dizziness. It also has antifungal and some antibacterial properties and is thus classified as an antifungal for topical use by the WHO. The major adverse effect from this preservative on skin is allergic contact sensitivity. Systemic intoxication from transdermal use has not been

neg: Diazepam the anticonvulsant effects. Diazepam is used for the emergency treatment of eclampsia, when IV magnesium sulfate and blood-pressure control measures have failed. Benzodiazepines do not have any pain-relieving properties themselves, and are generally recommended to avoid in individuals with pain. However, benzodiazepines such as diazepam can be used for their muscle-relaxant properties to alleviate pain caused by muscle spasms and various dystonias, including blepharospasm. Tolerance often develops to the muscle relaxant effects of benzodiazepines such as diazepam. Baclofen or tizanidine is sometimes used as an alternative to diazepam. Diazepam is marketed in over 500 brands throughout the world. It is

neg: Anticonvulsant or midazolam is usually tried first. Other barbiturates only have an anticonvulsant effect at anaesthetic doses. The benzodiazepines are a class of drugs with hypnotic, anxiolytic, anticonvulsive, amnestic and muscle relaxant properties. Benzodiazepines act as a central nervous system depressant. The relative strength of each of these properties in any given benzodiazepine varies greatly and influences the indications for which it is prescribed. Long-term use can be problematic due to the development of tolerance to the anticonvulsant effects and dependency. Of the many drugs in this class, only a few are used to treat epilepsy: The following benzodiazepines are used

neg: Xylazine where it is diverted from stocks used by equine veterinarians and used as a cutting agent for heroin. Xylazine is often used as a sedative, muscle relaxant, and analgesic. It is frequently used in the treatment of tetanus. Xylazine is very similar to drugs such as phenothiazine, tricyclic antidepressants, and clonidine. As an anesthetic, it is typically used in conjunction with ketamine. Xylazine appears to reduce sensitivity to insulin and glucose uptake in humans. Yohimbine has been used to decrease glucose levels to a healthy level. In clinical settings, Yohimbine can reverse the adverse effects of xylazine if administered intravenously

neg: Neuromuscular-blocking drug a depolarizing effect. Cations must be able to flow through the trans-membrane tube of the ion-channel to depolarize the endplate. Small molecules may be rigid and potent but unable to occupy or block the area between the receptive sites. Large molecules, on the other hand, may bind to both receptive sites and hinder depolarizing cations independent of whether the ion-channel is open or closed below. Having a lipophilic surface pointed towards the synapse enhances this effect by repelling cations. The importance of this effect varies between different muscle relaxants and classifying depolarizing from non-depolarizing blocks is a complex issue. The

neg: Tofisopam action for its various therapeutic effects, and this action has been proposed to make tofisopam potentially useful as a treatment for schizophrenia. Tofisopam has been shown to act as an inhibitor of the liver enzyme CYP3A4, and this could cause dangerous drug interactions with other medications metabolised by this enzyme, although the clinical significance of these findings remains unclear. Tofisopam Tofisopam (Emandaxin, Grandaxin, Sériel) is an anxiolytic that is marketed in several European countries. Chemically, it is a 2,3-benzodiazepine. Unlike other anxiolytic benzodiazepines (which are generally 1,4- or 1,5-substituted) however, tofisopam does not have anticonvulsant, sedative, skeletal muscle relaxant, motor

neg: Muscle relaxant women, or people who suffer depression or for those with a history of drug or alcohol addiction. Because of the enhancement of inhibition in the CNS, most spasmolytic agents have the side effects of sedation, drowsiness and may cause dependence with long-term use. Several of these agents also have abuse potential, and their prescription is strictly controlled. The benzodiazepines, such as diazepam, interact with the GABA receptor in the central nervous system. While it can be used in patients with muscle spasm of almost any origin, it produces sedation in most individuals at the doses required to reduce muscle tone.

neg: Neuromuscular-blocking drug not clear. Metabolism and Hofmann elimination Deacetylating vecuronium at position 3 results in a very active metabolite. In the case of rapacuronium the 3-deacylated metabolite is even more potent than rapacuronium. As long as the D-ring acetylcholine moiety is unchanged they retain their muscle relaxing effect. "Mono"-quaternary aminosteroids produced with deacylation in position 17 on the other hand are generally weak muscle relaxants. In the development of atracurium the main idea was to make use of Hofmann elimination of the muscle relaxant "in vivo". When working with bisbenzyl-isoquinolinium types of molecules, inserting proper features into the molecule such as an

neg: Clorazepate Clorazepate Clorazepate, sold under the brand names Tranxene among others, is a benzodiazepine medication. It possesses anxiolytic, anticonvulsant, sedative, hypnotic, and skeletal muscle relaxant properties. Clorazepate is an unusually long-lasting benzodiazepine and serves as a majoritive prodrug for the equally long-lasting desmethyldiazepam, which is rapidly produced as an active metabolite. Desmethyldiazepam is responsible for most of the therapeutic effects of clorazepate. Clorazepate is used in the treatment of anxiety disorders and insomnia. It may also be prescribed as an anticonvulsant or muscle relaxant. It is also used as a premedication. Clorazepate is prescribed principally in the treatment of alcohol withdrawal

neg: Neostigmine is used to improve muscle tone in people with myasthenia gravis, and also to reverse the effects of non-depolarizing muscle relaxants such as rocuronium and vecuronium at the end of an operation, usually in a dose of 25 to 50 μg per kilogram. Another indication for use is the conservative management of acute colonic pseudo-obstruction, or Ogilvie's syndrome, in which patients get massive colonic dilatation in the absence of a true mechanical obstruction. Hospitals sometimes administer a solution containing neostigmine intravenously to delay the effects of envenomation through snakebite. Some promising research results have also been reported for administering the

neg: Abecarnil and it looks likely to be developed for use both in the treatment of anxiety, and as a less addictive substitute drug for the treatment of benzodiazepine and alcohol addiction. Abecarnil may also have fewer problems of tolerance and withdrawal problems compared to nonselective full agonist benzodiazepine acting drugs. Abecarnil is a relatively subtype-selective drug which produces primarily anxiolytic effects, with comparatively less sedative or muscle relaxant properties, and does not significantly potentiate the effects of alcohol. The abuse potential of abecarnil is thought to be less than that of benzodiazepines, with only mild withdrawal symptoms noted after abrupt discontinuation

neg: Metaxalone Metaxalone Metaxalone (marketed by King Pharmaceuticals under the brand name Skelaxin) is a muscle relaxant used to relax muscles and relieve pain caused by strains, sprains, and other musculoskeletal conditions. Its exact mechanism of action is not known, but it may be due to general central nervous system depression. It is considered to be a moderately strong muscle relaxant, with relatively low incidence of side effects. Skelaxin is available in an 800 mg scored tablet. Possible side effects include nausea, vomiting, drowsiness and CNS side effects, such as dizziness, headache, and irritability. The metabolism of metaxalone involves the liver cytochrome

neg: Metaxalone for few analytical methods Metaxalone Metaxalone (marketed by King Pharmaceuticals under the brand name Skelaxin) is a muscle relaxant used to relax muscles and relieve pain caused by strains, sprains, and other musculoskeletal conditions. Its exact mechanism of action is not known, but it may be due to general central nervous system depression. It is considered to be a moderately strong muscle relaxant, with relatively low incidence of side effects. Skelaxin is available in an 800 mg scored tablet. Possible side effects include nausea, vomiting, drowsiness and CNS side effects, such as dizziness, headache, and irritability. The metabolism of metaxalone

neg: Chlorzoxazone Like metaxalone, no specific mechanism of action has been identified for chlorzoxazone, with general central nervous system depression being the only currently accepted aspect to its medical benefits. Search for the exact mechanism of action is ongoing but limited due to the existence of more-effective safe muscle relaxers (ex. diazepam, cyclobenzaprine, tizanidine) greatly limiting the potential benefit of identifying novel compounds which share chlozoxazone's mechanism of action. As of 2015 the cost for a typical course of medication in the United States is less than 25 USD. Chlorzoxazone Chlorzoxazone (INN) is a centrally acting muscle relaxant used to treat muscle

neg: Fabomotizole Fabomotizole Fabomotizole (INN) (brand name Afobazole) is an anxiolytic drug launched in Russia in the early 2000s. It produces anxiolytic and neuroprotective effects without any sedative or muscle relaxant actions. Its mechanism of action remains poorly defined however, with GABAergic, NGF- and BDNF-release-promoting, MT1 receptor agonism, MT3 receptor antagonism, and sigma agonism suggested as potential mechanisms. Fabomotizole was shown to inhibit MAO-A reversibly and there might be also some involvement with serotonin receptors. Clinical trials have shown fabomotizole to be well tolerated and reasonably effective for the treatment of anxiety. Experiments of mice have shown antimutagenic and antiteratogenic properties. Fabomotizole

neg: Xylazine and muscle relaxant in dogs, cats, horses, elk, fallow deer, mule deer, sika deer, and white-tailed deer. The sedative and analgesic effects of xylazine are related to central nervous system depression. Xylazine’s muscle relaxant effect inhibits the transmission of neural impulses in the central nervous system. In scientific research, xylazine is a component of the most common anesthetic, ketamine-xylazine, which is used in rats, mice, hamster, and guinea pigs. The accounts of the actions and uses of xylazine in animals were reported as early as the late 1960s and early 1970s. Since the early 2000s, xylazine has become popular as

neg: Y-23684 effects at low doses that cause little or no sedative side effects. It has been proposed for development for human medical use, but has not yet gone beyond animal tests. Y-23684 Y-23684 is an anxiolytic drug with a novel chemical structure, which is used in scientific research. It has similar effects to benzodiazepine drugs, but is structurally distinct and so is classed as a nonbenzodiazepine anxiolytic. Y-23684 is a nonselective partial agonist at GABA receptors. It has primarily anxiolytic and anticonvulsant effects, with sedative and muscle relaxant effects only appearing at higher doses. It produces little ataxia or potentiation of

neg: History of electroconvulsive therapy in the United Kingdom patient is given an anaesthetic and a muscle relaxant. A brief-pulse electric current of about 800 milliamperes is passed between two electrodes on the head for several seconds, causing a seizure. The resulting convulsion is modified by the muscle relaxant. ECT is usually given on an inpatient basis; about one in five treatments are given on an outpatient basis. Treatment is usually given twice a week (occasionally three times a week) for a total of 6–12 treatments, although courses may be longer or shorter. About 70 per cent of ECT patients are women. About 1,500 ECT patients a year in

neg: Camazepam Camazepam Camazepam is a benzodiazepine psychoactive drug, marketed under the brand names Albego, Limpidon and Paxor. It is the dimethyl carbamate ester of temazepam, a metabolite of diazepam. While it possesses anxiolytic, anticonvulsant, skeletal muscle relaxant and hypnotic properties it differs from other benzodiazepines in that its anxiolytic properties are particularly prominent but has comparatively limited anticonvulsant, hypnotic and skeletal muscle relaxant properties. Camazepam, like others benzodiazepines, produce a variety of therapeutic and adverse effects by binding to the benzodiazepine receptor site on the GABA receptor and modulating the function of the GABA receptor, the most prolific inhibitory receptor within

neg: Papaverine Merck (1794–1855), founder of the Merck corporation, a major German chemical and pharmaceutical company. Papaverine is approved to treat spasms of the gastrointestinal tract, bile ducts and ureter and for use as a cerebral and coronary vasodilator in subarachnoid hemorrhage (combined with balloon angioplasty) and coronary artery bypass surgery. Papaverine may also be used as a smooth muscle relaxant in microsurgery where it is applied directly to blood vessels. Papaverine is used as an erectile dysfunction drug, alone or sometimes in combination. Papaverine, when injected in penile tissue, causes direct smooth muscle relaxation and consequent filling of the corpus cavernosum

neg: Muscle relaxant as many synthetic derivatives, played a significant role in scientific experiments to determine the function of acetylcholine in neuromuscular transmission. By 1943, neuromuscular blocking drugs became established as muscle relaxants in the practice of anesthesia and surgery. The U.S. Food and Drug Administration (FDA) approved the use of carisoprodol in 1959, metaxalone in August 1962, and cyclobenzaprine in August 1977. Other skeletal muscle relaxants of that type used around the world come from a number of drug categories and other drugs used primarily for this indication include orphenadrine (anticholinergic), chlorzoxazone, tizanidine (clonidine relative), diazepam, tetrazepam and other benzodiazepines, mephenoxalone, methocarbamol,

neg: Bruce Lee May 10 or his death on July 20". Dr. R. R. Lycette, the clinical pathologist at Queen Elizabeth Hospital, reported at the coroner hearing that the death could not have been caused by cannabis. At the 1975 San Diego Comic-Con convention, Lee's friend Chuck Norris attributed his death to a reaction to the combination of the muscle-relaxant medication he had been taking since 1968 for a ruptured disc in his back and an "antibiotic" he was given for his headache on the night of his death. In a 2017 episode of the Reelz TV series "", forensic pathologist Dr. Michael

neg: Quazepam Quazepam is selective for type I benzodiazepine receptors containing the α subunit, similar to other drugs such as zaleplon and zolpidem. As a result, quazepam has little or no muscle relaxant properties. Most other benzodiazepines are unselective and bind to type1 GABA receptors and type2 GABA receptors. Type1 GABA receptors include the α subunit containing GABA receptors which are responsible for hypnotic properties of the drug. Type 2 receptors include the α, α and α subunits which are responsible for anxiolytic action, amnesia and muscle relaxant properties. Thus quazepam may have less side effects than other benzodiazepines but, it has

neg: Treatment of equine lameness pass effect. While pentoxyfylline has a better bioavailability after oral dosing, its absorption may decrease with repeated administration. Pentoxyfilline has been shown to reduce lameness in horses with experimentally induced laminitis and has inhibitory effects on matrix metalloproteinases (MMP), so it may be beneficial for laminitis treatment despite its uncertain effects on digital blood flow. Methocarbamol, sold under the trade name Robaxin, is a muscle relaxant commonly used in horses to treat muscle pain secondary to spasticity, tetanus, or tying-up. Both oral and injectable forms are on the market. Its use is regulated by many equine competitive governing bodies, since

neg: Benzodiazepine compound left over from the discontinued project while spring-cleaning in the lab. This compound, later named chlordiazepoxide, had not been tested in 1955 because of Sternbach's focus on other issues. Expecting pharmacology results to be negative, and hoping to publish the chemistry-related findings, researchers submitted it for a standard battery of animal tests. However, the compound showed very strong sedative, anticonvulsant, and muscle relaxant effects. These impressive clinical findings led to its speedy introduction throughout the world in 1960 under the brand name "Librium". Following chlordiazepoxide, diazepam marketed by Hoffmann–La Roche under the brand name "Valium" in 1963, and for

neg: Chemical synapse synaptic function, and often are restricted to synapses that use a specific neurotransmitter. For example, curare is a poison that stops acetylcholine from depolarizing the postsynaptic membrane, causing paralysis. Strychnine blocks the inhibitory effects of the neurotransmitter glycine, which causes the body to pick up and react to weaker and previously ignored stimuli, resulting in uncontrollable muscle spasms. Morphine acts on synapses that use endorphin neurotransmitters, and alcohol increases the inhibitory effects of the neurotransmitter GABA. LSD interferes with synapses that use the neurotransmitter serotonin. Cocaine blocks reuptake of dopamine and therefore increases its effects. During the 1950s, Bernard Katz

neg: Azathioprine other hand, low doses of allopurinol have been shown to safely enhance the efficacy of azathioprine, especially in inflammatory bowel disease non-responders. This may still lead to lower lymphocyte counts and higher rates of infection, therefore the combination requires careful monitoring. Azathioprine decreases the effects of the anticoagulant warfarin and of non-depolarizing muscle relaxants, but increases the effect of depolarizing muscle relaxants. It can also interfere with niacin (vitamin B), resulting in at least one case to pellagra and fatal medullary aplasia. It has also been reported to cause vitamin B deficiency. Azathioprine can cause birth defects. A 2003 population-based

neg: Muscle relaxant to at least 1973. The term "spasmolytic" is also considered a synonym for antispasmodic. Spasmolytics such as carisoprodol, cyclobenzaprine, metaxalone, and methocarbamol are commonly prescribed for low back pain or neck pain, fibromyalgia, tension headaches and myofascial pain syndrome. However, they are not recommended as first-line agents; in acute low back pain, they are not more effective than paracetamol or nonsteroidal anti-inflammatory drugs (NSAIDs), and in fibromyalgia they are not more effective than antidepressants. Nevertheless, some (low-quality) evidence suggests muscle relaxants can add benefit to treatment with NSAIDs. In general, no high-quality evidence supports their use. No drug has been

neg: Tricaine mesylate Tricaine mesylate Tricaine mesylate (Tricaine methanesulfonate, TMS, MS-222), is white powder used for anesthesia, sedation, or euthanasia of fish. TMS is the only anesthetic licensed in the United States for fin fish that are intended for human consumption. The drug can have selective toxicity for poikilotherms due to their lower rate of metabolism in the liver. TMS is a muscle relaxant that operates by preventing action potentials. By blocking action potentials, no signals can be exchanged between the brain and the extremities. There will be no sensory input or muscle contractions which would have been caused by action potential, which

neg: Alverine Alverine Alverine is a drug used for functional gastrointestinal disorders. Alverine is a smooth muscle relaxant. Smooth muscle is a type of muscle that is not under voluntary control; it is the muscle present in places such as the gut and uterus. The side effects of alverine include: It was reported that alverine may induce toxic hepatitis. Alverine acts directly on the muscle in the gut, causing it to relax. This prevents the muscle spasms which occur in the gut in conditions such as irritable bowel syndrome and diverticular disease. Diverticular disease is a condition in which small pouches form

neg: Sugammadex Sugammadex Sugammadex (Org 25969, tradename Bridion) is an agent for reversal of neuromuscular blockade by the agent rocuronium in general anaesthesia. It is the first selective relaxant binding agent (SRBA). Sugammadex is used to reverse neuromuscular blockade after administration of non-depolarizing neuromuscular-blocking agents such as vecuronium or rocuronium. Sugammadex is a modified γ-cyclodextrin, with a lipophilic core and a hydrophilic periphery. This gamma cyclodextrin has been modified from its natural state by placing eight carboxyl thio ether groups at the sixth carbon positions. These extensions extend the cavity size allowing greater encapsulation of the rocuronium molecule. These negatively charged extensions

neg: Clenbuterol which body fat is metabolized while increasing the body's basal metabolic rate (BMR). It is commonly used for smooth muscle-relaxant properties as a bronchodilator and tocolytic. It is classified by the World Athletic Doping Association as an anabolic agent, not as a β agonist. Clenbuterol is also prescribed for treatment of respiratory diseases horses, and not in dogs and cats; it is illegal in most countries to use in livestock used for food. Clenbuterol is approved for use in some countries, free or via prescription, as a bronchodilator for asthma patients. Clenbuterol is not an ingredient of any therapeutic drug

neg: Myofascial trigger point is because a muscle spasm refers to the entire muscle contracting whereas the local twitch response also refers to the entire muscle but only involves a small twitch, no contraction. Among physicians, various specialists might use trigger point therapy. These include physiatrists (physicians specializing in physical medicine and rehabilitation), family medicine, and orthopedics. Osteopathic as well as chiropractic schools also include trigger points in their training. Other health professionals, such as athletic trainers, occupational therapists, physiotherapists, acupuncturists, massage therapists and structural integrators are also aware of these ideas and many of them make use of trigger points in their clinical

neg: Chlorpromazine of chlorpromazine has generally been superseded by use of acepromazine. Chlorpromazine may be used as an antiemetic in dogs and cats, or, less often, as sedative prior to anesthesia. In horses, it often causes ataxia and lethargy, and is therefore seldom used. It is commonly used to decrease nausea in animals that are too young for other common anti-emetics. It is also sometimes used as a preanesthetic and muscle relaxant in cattle, swine, sheep, and goats. The use of chlorpromazine in food-producing animals is not permitted in the EU, as a maximum residue limit could not be determined following assessment

neg: Muscle contraction ryanodine receptor, RyR) and voltage-gated L-type calcium channels (identified as dihydropyridine receptors, DHPRs). DHPRs are located on the sarcolemma (which includes the surface sarcolemma and the transverse tubules), while the RyRs reside across the SR membrane. The close apposition of a transverse tubule and two SR regions containing RyRs is described as a triad and is predominantly where excitation–contraction coupling takes place. Excitation–contraction coupling occurs when depolarization of skeletal muscle cell results in a muscle action potential, which spreads across the cell surface and into the muscle fiber's network of T-tubules, thereby depolarizing the inner portion of the muscle fiber.

neg: Suxethonium chloride storage issue is a concern (e.g. by the military, rural locations, 3rd world countries). The most recent reference to it in Medline is 1976, but it is occasionally mentioned in passing in other journals. Suxethonium chloride Suxethonium (trade name: "Brevidil-E") is a depolarising muscle relaxant which is presented as a dry powder in an ampoule. This is re-constituted with sterile water prior to use. It is available in Australia as a schedule 4 drug, and the US. It has some advantages over suxamethonium: The last advantage was what keeps it in occasional use. In the UK, it was used by

neg: Benzodiazepine dependence (Librium). Symptom severity is worse with the use of high doses, or with benzodiazepines of high potency or short half-life. Other cross-tolerant sedative hypnotics, such as barbiturates or alcohol, increase the risk of benzodiazepine dependence. Similar to opioids' use for pain, therapeutic use of benzodiazepines rarely leads to substance abuse. Tolerance develops rapidly to the sleep-inducing effects of benzodiazepines. The anticonvulsant and muscle-relaxant effects last for a few weeks before tolerance develops in most individuals. Tolerance results in a desensitization of GABA receptors and an increased sensitization of the excitatory neurotransmitter system, glutamate such as NMDA glutamate receptors. These changes