Interactions of alcuronium, TMB-8, and other allosteric ligands with muscarinic acetylcholine receptors: studies with chimeric receptors. (1/14)

A series of ligands that allosterically modulate the binding of classical ligands to muscarinic receptors was evaluated at wild-type and chimeric receptors. All of the ligands studied had highest affinity toward the M(2) subtype and lowest affinity toward the M(5) subtype. The chimeric receptors were mostly M(5) sequence; the amount of M(2) sequence ranged from about 6 to just under 30%. Alcuronium and TMB-8 had much higher affinity for the chimeric receptor that included the M(2) second outer loop of the receptor plus flanking regions of TM4 and TM5 than for any of the other chimeric receptors (the affinities of which remained similar to that of the M(5) subtype). However, this chimera retained the negative cooperativity between alcuronium and the classical antagonist N-methylscopolamine that is characteristic of M(5) (these ligands are positively cooperative at M(2)). Verapamil, tetrahydroaminoacridine, and d-tubocurarine were also sensitive to that chimeric substitution, although verapamil and tetrahydroaminoacridine had even higher affinity for a chimera with M(2) sequence in TM7. None of these ligands shared gallamine's sensitivity to a region of the third outer loop, but studies in which obidoxime reversed the allosteric effects of gallamine and other ligands suggested that they nevertheless compete for a common site. In summary, although the present data are consistent with previous studies that have suggested that allosteric ligands bind to the outermost regions of muscarinic receptors, it appears that different allosteric ligands may derive subtype selectivity from different regions of the receptor.  (+info)

Changes of cooperativity between N-methylscopolamine and allosteric modulators alcuronium and gallamine induced by mutations of external loops of muscarinic M(3) receptors. (2/14)

To clarify the involvement of specific domains of muscarinic receptors in the action of allosteric modulators, muscarinic M(3) receptors (on which allosteric interactions are weak) were genetically modified to become more similar to M(2) receptors (on which allosteric interactions are strong) and were expressed in COS-7 cells. Affinity for allosteric modulator gallamine was enhanced 25- to 50-fold by modifications of the third external loop (o3) and the negative effect of gallamine on the affinity for classical antagonist N-[(3)H]methylscopolamine ([(3)H]NMS) was augmented. Affinity for alcuronium became 3-fold higher after the o3 loop of M(3) receptors was made identical with the o3 loop of M(2) receptors, and alcuronium acquired positive influence on the affinity for [(3)H]NMS. This is the first instance of inducing positive cooperativity on muscarinic receptors by genetic manipulation. Transferring whole o2 loop from M(2) to M(3) receptors substantially enhanced affinities for gallamine and alcuronium without augmenting their negative action on [(3)H]NMS binding. In contrast, effects of simply adding two negative charges into the o2 loop of M(3) receptors were small. Removal of Arg from o1 loop abolished the negative effect of gallamine but not of alcuronium on [(3)H]NMS binding at equilibrium. Data point to an important role of o3 loop in the mechanism of the positive and negative cooperativity between [(3)H]NMS and alcuronium and gallamine, respectively, and in the binding of both modulators to M(2) receptors and reveal independence between mutation-induced changes in the affinity for a modulator and in the magnitude and direction of the allosteric effect of the modulator.  (+info)

Allosteric modulation of muscarinic receptor signaling: alcuronium-induced conversion of pilocarpine from an agonist into an antagonist. (3/14)

Previous studies on allosteric interactions at muscarinic receptors have often focused on ligand-receptor binding interactions, because ligand binding seemed to reflect functional consequences. The prototypal allosteric agent alcuronium is known to bind with similar affinity to the M(2) subtype of muscarinic acetylcholine receptors whether or not the receptors are occupied by the agonist pilocarpine. To determine allosteric modulation of receptor signaling by alcuronium, the effects of pilocarpine were measured in contracting guinea pig left atria and on G-protein coupling in M(2)-transfected Chinese hamster ovary (CHO) cell membranes. Alcuronium dose-dependently suppressed pilocarpine-induced reduction of isometric contraction force in atria (pIC(50, Alc) = 5.63) without any effect on the EC(50) of pilocarpine, consistent with an allosteric mechanism. In contrast, alcuronium shifted the concentration-effect curve of the agonist oxotremorine M to the right without affecting the maximal effect, in a formally competitive manner (pK(A, Alc) = 5.54). If pilocarpine remained receptor bound in the presence of alcuronium, this indicates that pilocarpine can no longer act as an agonist. In support of this hypothesis, pilocarpine acted as a competitive antagonist against oxotremorine M in the presence of 10 microM alcuronium. Measuring guanosine 5'-O-(3-[(35)S]thio)triphosphate ([(35)S]GTPgammaS) binding in CHO-M(2) membranes yielded similar results. Alcuronium suppressed pilocarpine-induced stimulation of [(35)S]GTPgammaS binding (pIC(50, Alc) = 5.47) without shift in EC(50), whereas it competitively shifted the response to oxotremorine M (pK(A, Alc) = 5.97). [(3)H]Oxotremorine M binding data corresponded with the functional findings. In conclusion, alcuronium converted the agonist pilocarpine into an antagonist-a novel type of functional allosteric interaction.  (+info)

Regulation of M2 muscarinic acetylcholine receptor expression and signaling by prolonged exposure to allosteric modulators. (4/14)

The effects of prolonged exposure of M(2) muscarinic acetylcholine receptors (mAChRs), stably expressed in Chinese hamster ovary cells, to the allosteric modulators gallamine, alcuronium, and heptane-1,7-bis (dimethyl-3'-phthalimidopropyl)-ammonium bromide (C(7)/3'-phth) were compared with the effects of the agonist carbachol (CCh) and antagonists atropine and N-methylscopolamine (NMS). Intact cell saturation binding assays using [(3)H]NMS found that pretreatment of the cells for 24 h with CCh caused a significant down-regulation of receptor number, whereas atropine, NMS, and all three allosteric modulators caused receptor up-regulation. Functional assays using a cytosensor microphysiometer to measure whole-cell metabolic rate found no acute effects of gallamine on receptor signaling, whereas atropine seemed to behave as an inverse agonist. Pretreatment of the cells with gallamine (20 microM) or atropine (20 nM) resulted in a significant enhancement of the maximal effect evoked by CCh. In contrast, CCh (100 microM) pretreatment resulted in a significant reduction in maximal receptor signaling capacity. Time-course experiments revealed that the effects of atropine and gallamine on receptor up-regulation are only visualized after at least 12-h ligand exposure, compared with the more rapid effects of CCh, which achieve steady-state down-regulation within 90 min. Additional experiments monitoring CCh-mediated M(2) mAChR internalization in the presence of gallamine revealed that part of the mechanism underlying the effects of the modulator on receptor expression may involve a change in receptor internalization properties. These findings suggest that, like orthosteric ligands, G protein-coupled receptor allosteric modulators also are able to mediate long-term effects on receptor regulation.  (+info)

Interaction of competitive antagonists: the anti-curare action of hexamethonium and other antagonists at the skeletal neuromuscular junction. (5/14)

1. In the rat isolated diaphragm preparation hexamethonium and other low potency competitive antagonists of acetylcholine (ACh), including gallamine and hyoscine butylbromide, reverse block by the potent antagonists tubocurarine, pancuronium and alcuronium. 2. In the presence of tubocurarine, hexamethonium increases the amplitude of the end-plate potential without increasing the quantal content. It enhances the response to ACh applied iontophoretically to the end-plate but does not enhance the response to ACh applied in the bath. 3. The anti-curare effect of hexamethonium is abolished in the diaphragm of the rat, guinea-pig and mouse by inhibitors of acetylcholinesterase. The effect is not observed in the indirectly stimulated toad sartorius muscle. 4. The effect is explained if tubocurarine does not dissociate appreciably in the time taken for ACh to achieve high occupancy of receptors, so that a fraction of receptors is completely excluded from occupation by ACh. Equilibration with hexamethonium reduces the fraction excluded by tubocurarine and the transmitter now competes with hexamethonium for more receptors and produces a larger response. 5. On the basis of this explanation the half-time for dissociation of tubocurarine must be about 1 millisecond. It follows that tubocurarine does not act competitively with ACh at synapses when transmitter action is sufficiently brief, and that its binding to the receptor is probably diffusion-limited.  (+info)

The impact of orthosteric radioligand depletion on the quantification of allosteric modulator interactions. (6/14)

 (+info)

Measurement of functional residual capacity by sulfur hexafluoride washout. (7/14)

Measurement of functional residual capacity (FRC) by the open-circuit multiple breath tracer gas washout technique is an established method. A system based upon washout of sulfur hexafluoride (SF6) during mechanical ventilation is described. The central unit in the system is a sensitive and rapid-response infrared SF6 analyzer. SF6 is washed in until the alveolar concentration of SF6 is 0.5%, a concentration so low that the supply of other gases is hardly influenced. During washout, the flow of SF6 from the lungs is calculated by a computer every 10 ms from signals representing expiratory flow and SF6 concentration. The total volume of SF6, washed out, is calculated by integration of SF6 flow. Since the alveolar concentration at the end of washin is known, the lung volume may be obtained. The measurement procedure is highly automated and the result is presented by the computer immediately after washout. Accurate and reproducible results in model lung tests were obtained during air and N2O/O2 ventilation. Comparison with body plethysmography (FRCBOX) in eight sitting healthy subjects gave the following: FRCSF6 = 7 ml + 0.98 X FRCBOX, r = 0.99. Comparison with nitrogen washout (FRCN2) in five postoperative patients gave the following: FRCSF6 = 59 ml + 0.97 X FRCN2, r = 0.97. FRCSF6 during N2O/O2 ventilation was the same as during air/O2 ventilation in a group of paralyzed patients. The measurement system has not been tested in patients with obstructive lung disease.  (+info)

Alcuronium kinetics in patients undergoing cardiopulmonary bypass surgery. (8/14)

1 The disposition of alcuronium was investigated in 10 patients undergoing surgery involving cardiopulmonary bypass (CPB) and compared with results from a group of non-cardiac patients studied previously. 2 After intravenous administration of a combined bolus and infusion dosage regimen, plasma concentrations fell in a bi-exponential fashion to a mean value of 0.55 micrograms/ml immediately before the start of extracorporeal circulation. 3 During CPB an apparent steady-state of alcuronium was reached immediately after commencement of CPB, however plasma concentrations were some 50% higher than those noted prior to commencement of CPB and those predicted using previous pharmacokinetic data from normal surgical patients. 4 Once CPB was completed and the alcuronium infusion terminated, post-infusion alcuronium plasma concentrations again appeared to decline bi-exponentially with time. 5 Of the pharmacokinetic parameters which were calculated model-independently, the apparent volume of distribution (Vss) was unchanged (329 vs 313 ml/kg) and the elimination half-life (t1/2,z) (532 vs 199 min) was prolonged and the plasma clearance (CL) (0.8 vs 1.34 ml min-1kg-1) markedly reduced in these patients compared to non-cardiac surgical patients. 6 As a result of these changes in alcuronium concentration during CPB and the diminished elimination of alcuronium following CPB, a closer monitoring of neuromuscular function may be necessary in cardiac patients undergoing CPB.  (+info)

*Alcuronium chloride

Alcuronium is a neuromuscular blocking (NMB) agent, alternatively referred to as a skeletal muscle relaxant. It is a semi- ... The major disadvantage of alcuronium is that it elicits a vagolytic effect produced by a selective atropine-like blockade of ... Maass A, Mohr K (1996). "Opposite effects of alcuronium on agonist and on antagonist binding to muscarinic receptors". Eur J ... Zahn K, Eckstein N, Tränkle C, Sadée W, Mohr K (2002). "Allosteric modulation of muscarinic receptor signaling: alcuronium- ...

*Tubocurarine chloride

Coleman AJ, Downing JW, Leary WP, Moyes DG (1972). "The immediate cardiovascular effects of pancuronium, alcuronium and ...

*Atracurium besilate

Yeung ML, Ng LY, Koo AW (Feb 1979). "Severe bronchospasm in an asthmatic patient following alcuronium and D-tubocurarine". ... as well as alcuronium, pancuronium, vecuronium, and gallamine. Seizures rarely occur. Because atracurium undergoes Hofmann ...

*Lethal injection

Then, 45 mg alcuronium chloride (Alloferin) or 18 mg pancuronium bromide (Pavulon) is injected. To ensure optimal availability ... In severe hepatitis or cirrhosis of the liver, alcuronium is the agent of first choice. Intravenous administration is the most ...

*Wieland-Gumlich aldehyde

The Wieland-Gumlich aldehyde has been used in the industrial synthesis of alcuronium chloride (Alloferin) via dimerization. ...

*Archie Brain

In 1982, he had his first publication: a letter to the editor suggesting that alcuronium should be used instead of ...

*Pentobarbital

... followed by bromide of alcuronium- or pancuronium-induced respiratory arrest. A concentrated oral solution of 100 mL containing ...

*List of drugs: Al

... the type known as ethanol Alcomicin Alconefrinasal Solution alcuronium chloride (INN) Aldactazide Aldactone Aldara (3m), also ...

*List of MeSH codes (D03)

... alcuronium MeSH D03.132.436.255.847 --- tubocurarine MeSH D03.132.436.444 --- harmaline MeSH D03.132.436.477 --- harmine MeSH ... alcuronium MeSH D03.438.473.402.255.847 --- tubocurarine MeSH D03.438.473.402.444 --- harmaline MeSH D03.438.473.402.477 --- ...

*ATC code M03

M03AA01 Alcuronium M03AA02 Tubocurarine M03AA04 Dimethyltubocurarine M03AB01 Suxamethonium M03AC01 Pancuronium M03AC02 ...

*Anesthetic

Short acting Mivacurium Rapacuronium Intermediate acting Atracurium Cisatracurium Rocuronium Vecuronium Long acting Alcuronium ...
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Alcuronium allosterically increases the affinity of cardiac muscarinic receptors for methyl-N-scopolamine (NMS), whereas gallamine has the opposite effect. We discovered that strychnine also increases the affinity of muscarinic receptors in rat heart atria for NMS. It is not known whether the positive and the negative allosteric effectors bind to the same binding site. To investigate this question, we elaborated on a theoretical model predicting changes in the binding of a classic radiolabeled ligand occurring in the presence of a positive and a negative allosteric effector that compete for the allosteric binding site. The model is based on data obtained at equilibrium and avoids uncertainties associated with the use of nonequilibrium methods for the evaluation of interactions between allosteric ligands. We examined changes in the binding of [3H]NMS to membranes of rat heart atria exposed to various concentrations of a positive allosteric effector (alcuronium or strychnine) and of a negative ...
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Alcuronium Chloride - Drugs.comAlcuronium Chloride - Drugs.com

A list of US medications equivalent to Alcuronium Chloride is available on the Drugs.com website. ... Alcuronium Chloride is a medicine available in a number of countries worldwide. ...
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Alcuronium chloride definition | Drugs.comAlcuronium chloride definition | Drugs.com

Definition of alcuronium chloride. Provided by Stedmans medical dictionary and Drugs.com. Includes medical terms and ... alcuronium chloride. Pronunciation: al-kūr-ō′nē-yŭm klōr′īd. Definition: A skeletal muscle relaxant active as a nondepolarizing ...
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Alcuronium chloride- CAS Number 15180-03-7Alcuronium chloride- CAS Number 15180-03-7

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alcuronium | Ligand page | IUPHAR/BPS Guide to PHARMACOLOGYalcuronium | Ligand page | IUPHAR/BPS Guide to PHARMACOLOGY

alcuronium ligand page. Quantitative data and detailed annnotation of the targets of licensed and experimental drugs. ... There is some ambiguity as to the exact stereochemistry of alcuronium. CID 5360723 represents an alternative isomer.. ...
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Alcuronium chloride - WikipediaAlcuronium chloride - Wikipedia

Alcuronium is a neuromuscular blocking (NMB) agent, alternatively referred to as a skeletal muscle relaxant. It is a semi- ... The major disadvantage of alcuronium is that it elicits a vagolytic effect produced by a selective atropine-like blockade of ... Maass A, Mohr K (1996). "Opposite effects of alcuronium on agonist and on antagonist binding to muscarinic receptors". Eur J ... Zahn K, Eckstein N, Tränkle C, Sadée W, Mohr K (2002). "Allosteric modulation of muscarinic receptor signaling: alcuronium- ...
more infohttps://en.wikipedia.org/wiki/Alcuronium_chloride

The effect of halothane on the action of alcuronium in the dog  - Zurich Open Repository and ArchiveThe effect of halothane on the action of alcuronium in the dog - Zurich Open Repository and Archive

Jones, R S; Heckmann, Rudolf; Wuersch, W (1979). The effect of halothane on the action of alcuronium in the dog. Experientia, ... The effect of halothane on the action of alcuronium on neuromuscular transmission was studied in the intact dog. Electrical and ... The effect of halothane on the action of alcuronium on neuromuscular transmission was studied in the intact dog. Electrical and ... The effect of halothane on the action of alcuronium in the dog ... halothane prolonged the duration of action of alcuronium by ...
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Gentamicin (Injection Route) Description and Brand Names - Mayo ClinicGentamicin (Injection Route) Description and Brand Names - Mayo Clinic

If your or your childs symptoms do not improve within a few days, or if they become worse, check with your doctor. Using this medicine while you are pregnant can harm your unborn baby. Use an effective form of birth control to keep from getting pregnant. If you think you have become pregnant while using the medicine, tell your doctor right away. This medicine may cause serious allergic reactions, including anaphylaxis, which can be life-threatening and require immediate medical attention. Call your doctor right away if you or your child have itching; hives; hoarseness; shortness of breath; trouble breathing; trouble swallowing; or any swelling of your hands, face, or mouth after you receive this medicine. Stop using this medicine and check with your doctor right away if you or your child have sudden decrease in hearing or loss of hearing, which may be accompanied by dizziness and ringing in the ears. Tell your doctor if you or your child have dizziness or lightheadedness; feeling of constant ...
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Kanamycin (Injection Route) Description and Brand Names - Mayo ClinicKanamycin (Injection Route) Description and Brand Names - Mayo Clinic

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Hereditary Coproporphyria Treatment & Management: Approach Considerations, DietHereditary Coproporphyria Treatment & Management: Approach Considerations, Diet

Alcuronium *Alphaxalone Alphadolone Alprazolam Aluminium Preparations Amidopyrine Aminoglutethimide Aminophylline Amiodarone * ...
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Acute Intermittent Porphyria: Practice Essentials, Pathophysiology, EpidemiologyAcute Intermittent Porphyria: Practice Essentials, Pathophysiology, Epidemiology

Acute intermittent porphyria (AIP) is one of the porphyrias, a group of diseases involving defects in heme metabolism and that results in excessive secretion of porphyrins and porphyrin precursors. AIP manifests itself by abdomen pain, neuropathies, and constipation, but, unlike most types of porphyria, patients with AIP do not have a rash.
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Carindacillin - DrugBankCarindacillin - DrugBank

Alcuronium. The therapeutic efficacy of Alcuronium can be increased when used in combination with Carindacillin. ...
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Quaternary Ammonium Compounds - DrugBankQuaternary Ammonium Compounds - DrugBank

Alcuronium. Not Available. DB14006. Choline salicylate. The oral gel is indicated for the relief of pain and discomfort of ...
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Meylers Side Effects of Drugs - Elsevier Science & Technology - Literati by CredoMeyler's Side Effects of Drugs - Elsevier Science & Technology - Literati by Credo

This updated edition in the long standing series provides the latest information on many individual drugs, including the most complete coverage of their adverse reactions and interactions.
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Valeant Pharmaceuticals productsValeant Pharmaceuticals products

Alcuronium Chloride. Alloprin. Allopurinol. Alumpak. Aluminum Chloride. Aminophylline. Aminophylline. Amoxivet. Amoxicillin ...
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ICN Pharmaceuticals productsICN Pharmaceuticals products

Alcuronium Chloride. Alloferine. Alcuronium Chloride. Alloprin. Allopurinol. Amitriptyline. Amitriptyline Hydrochloride. ...
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Plus itPlus it

8; Table 2) were: 470 nM mecamylamine , 1.5 μM DHβE , 6.6 μM MLA , 11 μM hexamethonium , 21 μM lobeline ≥ 26 μM alcuronium ∼ 28 ... F/B ratios are between 1 and 2 for classic curarimimetics such as pancuronium, vecuronium, and alcuronium, suggesting close ... alcuronium (alc; ▾) and eserine (eser; ⋄). Log IC50 values and Hill coefficients (± S.E.M.) are provided in Table 1, and IC50 ... 760 μM alcuronium ∼ 980 μM vecuronium , 1.9 mM hexamethonium ∼ 2.3 mM pancuronium » 1 mM eserine (Fig. 6, Table 1). ...
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Tubocurarine chloride - WikipediaTubocurarine chloride - Wikipedia

Coleman AJ, Downing JW, Leary WP, Moyes DG (1972). "The immediate cardiovascular effects of pancuronium, alcuronium and ...
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Hydrocortisone (Injection route)Hydrocortisone (Injection route)

It is very important that your doctor check the progress of you or your child closely while you are receiving this medicine to make sure that this medicine is working properly. Blood and urine tests may be needed to check for unwanted effects. Using too much of this medicine or using it for a long time may increase your risk of having adrenal gland problems. Talk to your doctor right away if you have more than one of these symptoms while you are using this medicine: blurred vision, dizziness or fainting, a fast, irregular, or pounding heartbeat, increased thirst or urination, irritability, or unusual tiredness or weakness. This medicine may cause you to get more infections than usual. Avoid people who are sick or have infections and wash your hands often. If you are exposed to chickenpox or measles, tell your doctor right away. If you start to have fever, chills, sore throat, or any other signs of an infection, call your doctor right away. If you are using this medicine for a long time, tell ...
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Smooth muscle | definition of smooth muscle by Medical dictionarySmooth muscle | definition of smooth muscle by Medical dictionary

Include d-tubocurarine, alcuronium chloride, pancuronium, vecuronium, atracurium besylate, succinylcholine.. red muscle. type 1 ...
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Atrial myocytes | definition of Atrial myocytes by Medical dictionaryAtrial myocytes | definition of Atrial myocytes by Medical dictionary

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Tobradex (Tobramycin & Dexamethasone) Ophthalmic: Uses & DosageTobradex (Tobramycin & Dexamethasone) Ophthalmic: Uses & Dosage

Tobradex is a combination of an antibiotic and a corticosteroid. It is used in the eye to prevent permanent damage, which may occur with certain eye problems. This medicine is...
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Streptomycin (Streptomycin) Intramuscular: Uses, Dosage & Side EffectsStreptomycin (Streptomycin) Intramuscular: Uses, Dosage & Side Effects

Streptomycin injection is used to treat moderate to severe bacterial infections in many different parts of the body. Streptomycin belongs to the class of medicines known as aminoglycoside...
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  • Alcuronium is a neuromuscular blocking (NMB) agent, alternatively referred to as a skeletal muscle relaxant. (wikipedia.org)