A non-depolarizing skeletal muscle relaxant similar to TUBOCURARINE. It is used as an anesthesia adjuvant.
A curare alkaloid that is a very potent competitive nicotinic antagonist at the neuromuscular junction.
A synthetic nondepolarizing blocking drug. The actions of gallamine triethiodide are similar to those of TUBOCURARINE, but this agent blocks the cardiac vagus and may cause sinus tachycardia and, occasionally, hypertension and increased cardiac output. It should be used cautiously in patients at risk from increased heart rate but may be preferred for patients with bradycardia. (From AMA Drug Evaluations Annual, 1992, p198)
A muscarinic antagonist used to study binding characteristics of muscarinic cholinergic receptors.
Agents that inhibit the actions of the parasympathetic nervous system. The major group of drugs used therapeutically for this purpose is the MUSCARINIC ANTAGONISTS.
The modification of the reactivity of ENZYMES by the binding of effectors to sites (ALLOSTERIC SITES) on the enzymes other than the substrate BINDING SITES.
One of the two major classes of cholinergic receptors. Muscarinic receptors were originally defined by their preference for MUSCARINE over NICOTINE. There are several subtypes (usually M1, M2, M3....) that are characterized by their cellular actions, pharmacology, and molecular biology.
An unnaturally deep or rough quality of voice.
An imprecise term which may refer to a sense of spatial disorientation, motion of the environment, or lightheadedness.
Spherical particles of nanometer dimensions.
An acute hypersensitivity reaction due to exposure to a previously encountered ANTIGEN. The reaction may include rapidly progressing URTICARIA, respiratory distress, vascular collapse, systemic SHOCK, and death.
A syndrome of ORTHOSTATIC INTOLERANCE combined with excessive upright TACHYCARDIA, and usually without associated ORTHOSTATIC HYPOTENSION. All variants have in common an excessively reduced venous return to the heart (central HYPOVOLEMIA) while upright.
Forceful administration under the skin of liquid medication, nutrient, or other fluid through a hollow needle piercing the skin.
A general term for the complete or partial loss of the ability to hear from one or both ears.
An autosomal dominant porphyria that is due to a deficiency of COPROPORPHYRINOGEN OXIDASE in the LIVER, the sixth enzyme in the 8-enzyme biosynthetic pathway of HEME. Clinical features include both neurological symptoms and cutaneous lesions. Patients excrete increased levels of porphyrin precursors, 5-AMINOLEVULINATE and COPROPORPHYRINS.
Porphyrins with four methyl and four propionic acid side chains attached to the pyrrole rings. Elevated levels of Coproporphyrin III in the urine and feces are major findings in patients with HEREDITARY COPROPORPHYRIA.
An enzyme that catalyzes the oxidative decarboxylation of coproporphyrinogen III to protoporphyrinogen IX by the conversion of two propionate groups to two vinyl groups. It is the sixth enzyme in the 8-enzyme biosynthetic pathway of HEME, and is encoded by CPO gene. Mutations of CPO gene result in HEREDITARY COPROPORPHYRIA.
A group of metabolic diseases due to deficiency of one of a number of LIVER enzymes in the biosynthetic pathway of HEME. They are characterized by the accumulation and increased excretion of PORPHYRINS or its precursors. Clinical features include neurological symptoms (PORPHYRIA, ACUTE INTERMITTENT), cutaneous lesions due to photosensitivity (PORPHYRIA CUTANEA TARDA), or both (HEREDITARY COPROPORPHYRIA). Hepatic porphyrias can be hereditary or acquired as a result of toxicity to the hepatic tissues.
A diverse group of metabolic diseases characterized by errors in the biosynthetic pathway of HEME in the LIVER, the BONE MARROW, or both. They are classified by the deficiency of specific enzymes, the tissue site of enzyme defect, or the clinical features that include neurological (acute) or cutaneous (skin lesions). Porphyrias can be hereditary or acquired as a result of toxicity to the hepatic or erythropoietic marrow tissues.
A group of compounds containing the porphin structure, four pyrrole rings connected by methine bridges in a cyclic configuration to which a variety of side chains are attached. The nature of the side chain is indicated by a prefix, as uroporphyrin, hematoporphyrin, etc. The porphyrins, in combination with iron, form the heme component in biologically significant compounds such as hemoglobin and myoglobin.
Colorless reduced precursors of porphyrins in which the pyrrole rings are linked by methylene (-CH2-) bridges.
Authoritative treatises on drugs and preparations, their description, formulation, analytic composition, physical constants, main chemical properties used in identification, standards for strength, purity, and dosage, chemical tests for determining identity and purity, etc. They are usually published under governmental jurisdiction (e.g., USP, the United States Pharmacopoeia; BP, British Pharmacopoeia; P. Helv., the Swiss Pharmacopoeia). They differ from FORMULARIES in that they are far more complete: formularies tend to be mere listings of formulas and prescriptions.
Disorders that result from the intended use of PHARMACEUTICAL PREPARATIONS. Included in this heading are a broad variety of chemically-induced adverse conditions due to toxicity, DRUG INTERACTIONS, and metabolic effects of pharmaceuticals.
The homogeneous mixtures formed by the mixing of a solid, liquid, or gaseous substance (solute) with a liquid (the solvent), from which the dissolved substances can be recovered by physical processes. (From Grant & Hackh's Chemical Dictionary, 5th ed)
Introduction of substances into the body using a needle and syringe.
The long-term (minutes to hours) administration of a fluid into the vein through venipuncture, either by letting the fluid flow by gravity or by pumping it.
The administration of liquid medication, nutrient, or other fluid through some other route than the alimentary canal, usually over minutes or hours, either by gravity flow or often by infusion pumping.
Fluid propulsion systems driven mechanically, electrically, or osmotically that are used to inject (or infuse) over time agents into a patient or experimental animal; used routinely in hospitals to maintain a patent intravenous line, to administer antineoplastic agents and other drugs in thromboembolism, heart disease, diabetes mellitus (INSULIN INFUSION SYSTEMS is also available), and other disorders.
A neuromuscular blocker and active ingredient in CURARE; plant based alkaloid of Menispermaceae.
Works containing information articles on subjects in every field of knowledge, usually arranged in alphabetical order, or a similar work limited to a special field or subject. (From The ALA Glossary of Library and Information Science, 1983)
Amphetamine metabolite with sympathomimetic effects. It is sometimes called alpha-methyltyramine, which may also refer to the meta isomer, gepefrine.
Plant extracts from several species, including genera STRYCHNOS and Chondodendron, which contain TETRAHYDROISOQUINOLINES that produce PARALYSIS of skeletal muscle. These extracts are toxic and must be used with the administration of artificial respiration.
Individuals whose ancestral origins are in the continents of the Americas.
A non-depolarizing neuromuscular blocking agent with short duration of action. Its lack of significant cardiovascular effects and its lack of dependence on good kidney function for elimination provide clinical advantage over alternate non-depolarizing neuromuscular blocking agents.
Drugs intended for human or veterinary use, presented in their finished dosage form. Included here are materials used in the preparation and/or formulation of the finished dosage form.
A notch receptor that interacts with a variety of ligands and regulates SIGNAL TRANSDUCTION PATHWAYS for multiple cellular processes. It is widely expressed during EMBRYOGENESIS and is essential for EMBRYONIC DEVELOPMENT.
A family of conserved cell surface receptors that contain EPIDERMAL GROWTH FACTOR repeats in their extracellular domain and ANKYRIN repeats in their cytoplasmic domains. The cytoplasmic domain of notch receptors is released upon ligand binding and translocates to the CELL NUCLEUS where it acts as transcription factor.
Process that is gone through in order for a drug to receive approval by a government regulatory agency. This includes any required pre-clinical or clinical testing, review, submission, and evaluation of the applications and test results, and post-marketing surveillance of the drug.
An agency of the PUBLIC HEALTH SERVICE concerned with the overall planning, promoting, and administering of programs pertaining to maintaining standards of quality of foods, drugs, therapeutic devices, etc.
That segment of commercial enterprise devoted to the design, development, and manufacture of chemical products for use in the diagnosis and treatment of disease, disability, or other dysfunction, or to improve function.
Conferences, conventions or formal meetings usually attended by delegates representing a special field of interest.
A bibliographic database that includes MEDLINE as its primary subset. It is produced by the National Center for Biotechnology Information (NCBI), part of the NATIONAL LIBRARY OF MEDICINE. PubMed, which is searchable through NLM's Web site, also includes access to additional citations to selected life sciences journals not in MEDLINE, and links to other resources such as the full-text of articles at participating publishers' Web sites, NCBI's molecular biology databases, and PubMed Central.
A publication issued at stated, more or less regular, intervals.
"The business or profession of the commercial production and issuance of literature" (Webster's 3d). It includes the publisher, publication processes, editing and editors. Production may be by conventional printing methods or by electronic publishing.
The premier bibliographic database of the NATIONAL LIBRARY OF MEDICINE. MEDLINE® (MEDLARS Online) is the primary subset of PUBMED and can be searched on NLM's Web site in PubMed or the NLM Gateway. MEDLINE references are indexed with MEDICAL SUBJECT HEADINGS (MeSH).
Publications in any medium issued in successive parts bearing numerical or chronological designations and intended to be continued indefinitely. (ALA Glossary of Library and Information Science, 1983, p203)
All of the divisions of the natural sciences dealing with the various aspects of the phenomena of life and vital processes. The concept includes anatomy and physiology, biochemistry and biophysics, and the biology of animals, plants, and microorganisms. It should be differentiated from BIOLOGY, one of its subdivisions, concerned specifically with the origin and life processes of living organisms.
Databases devoted to knowledge about specific chemicals.
Macrolide antifungal antibiotic produced by Streptomyces nodosus obtained from soil of the Orinoco river region of Venezuela.
Any liquid or solid preparation made specifically for the growth, storage, or transport of microorganisms or other types of cells. The variety of media that exist allow for the culturing of specific microorganisms and cell types, such as differential media, selective media, test media, and defined media. Solid media consist of liquid media that have been solidified with an agent such as AGAR or GELATIN.
Cells that line the inner and outer surfaces of the body by forming cellular layers (EPITHELIUM) or masses. Epithelial cells lining the SKIN; the MOUTH; the NOSE; and the ANAL CANAL derive from ectoderm; those lining the RESPIRATORY SYSTEM and the DIGESTIVE SYSTEM derive from endoderm; others (CARDIOVASCULAR SYSTEM and LYMPHATIC SYSTEM) derive from mesoderm. Epithelial cells can be classified mainly by cell shape and function into squamous, glandular and transitional epithelial cells.
Established cell cultures that have the potential to propagate indefinitely.
An intermediate compound in the metabolism of carbohydrates, proteins, and fats. In thiamine deficiency, its oxidation is retarded and it accumulates in the tissues, especially in nervous structures. (From Stedman, 26th ed)
An antibiotic produced by the soil actinomycete Streptomyces griseus. It acts by inhibiting the initiation and elongation processes during protein synthesis.

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)

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Coleman AJ, Downing JW, Leary WP, Moyes DG (1972). "The immediate cardiovascular effects of pancuronium, alcuronium and ...
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 ...
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 ...
The Wieland-Gumlich aldehyde has been used in the industrial synthesis of alcuronium chloride (Alloferin) via dimerization. ...
Many other different structures have been used for their muscle relaxant effect such as alcuronium (alloferin), anatruxonium, ...
In 1982, he had his first publication: a letter to the editor suggesting that alcuronium should be used instead of ...
... the type known as ethanol Alcomicin Alconefrinasal Solution alcuronium chloride (INN) Aldactazide Aldactone Aldara (3m), also ...
... alcuronium MeSH D03.132.436.255.847 - tubocurarine MeSH D03.132.436.444 - harmaline MeSH D03.132.436.477 - harmine MeSH D03.132 ... alcuronium MeSH D03.438.473.402.255.847 - tubocurarine MeSH D03.438.473.402.444 - harmaline MeSH D03.438.473.402.477 - harmine ...
M03AA01 Alcuronium M03AA02 Tubocurarine M03AA04 Dimethyltubocurarine M03AB01 Suxamethonium M03AC01 Pancuronium M03AC02 ...
Short acting Mivacurium Rapacuronium Intermediate acting Atracurium Cisatracurium Rocuronium Vecuronium Long acting Alcuronium ...
... is a neuromuscular blocking (NMB) agent, alternatively referred to as a skeletal muscle relaxant. It is a ... 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- ...
Ji, Jianguo; Bunnelle, William H.; Anderson, David J.; Faltynek, Connie; Dyhring, Tino; Ahring, Philip K.; Rueter, Lynne E.; Curzon, Peter; Buckley, Michael J.; Marsh, Kennan C.; Kempf-Grote, Anita; Meyer, Michael D. (2007). "A-366833: A novel nicotinonitrile-substituted 3,6-diazabicyclo[3.2.0]-heptane α4β2 nicotinic acetylcholine receptor selective agonist: Synthesis, analgesic efficacy and tolerability profile in animal models". Biochemical Pharmacology. 74 (8): 1253-1262. doi:10.1016/j.bcp.2007.08.010. PMID 17854775 ...
InChI=1S/C48H74O14.C47H72O14/c1-11-25(2)43-28(5)17-18-47(62-43)23-34-20-33(61-47)16-15-27(4)42(26(3)13-12-14-32-24-55-45-40(49)29(6)19-35(46(51)58-34)48(32,45)52)59-39-22-37(54-10)44(31(8)57-39)60-38-21-36(53-9)41(50)30(7)56-38;1-24(2)41-27(5)16-17-46(61-41)22-33-19-32(60-46)15-14-26(4)42(25(3)12-11-13-31-23-54-44-39(48)28(6)18-34(45(50)57-33)47(31,44)51)58-38-21-36(53-10)43(30(8)56-38)59-37-20-35(52-9)40(49)29(7)55-37/h12-15,19,25-26,28,30-31,33-45,49-50,52H,11,16-18,20-24H2,1-10H3;11-14,18,24-25,27,29-30,32-44,48-49,51H,15-17,19-23H2,1-10H3/b13-12+,27-15+,32-14+;12-11+,26-14+,31-13+/t25-,26-,28-,30-,31-,33+,34-,35-,36-,37-,38-,39-,40+,41-,42-,43+,44-,45+,47+,48+;25-,27-,29-,30-,32+,33-,34-,35-,36-,37-,38-,39+,40-,41+,42-,43-,44+,46+,47+/m00/s1 ...
... (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 P450 system. Based on the information in the labeling, patients receiving metaxalone therapy and physicians prescribing metaxalone are directed to take precaution when coadministering it with other medications involving the P450 system.[1][2] Because of potential for side effects, this drug is considered high risk in the elderly. As of 2015[update] the ...
... (acetyl coenzyme A) is a molecule that participates in many biochemical reactions in protein, carbohydrate and lipid metabolism.[1] Its main function is to deliver the acetyl group to the citric acid cycle (Krebs cycle) to be oxidized for energy production. Coenzyme A (CoASH or CoA) consists of a β-mercaptoethylamine group linked to the vitamin pantothenic acid through an amide linkage [2] and 3'-phosphorylated ADP. The acetyl group (indicated in blue in the structural diagram on the right) of acetyl-CoA is linked to the sulfhydryl substituent of the β-mercaptoethylamine group. This thioester linkage is a "high energy" bond, which is particularly reactive. Hydrolysis of the thioester bond is exergonic (−31.5 kJ/mol). CoA is acetylated to acetyl-CoA by the breakdown of carbohydrates through glycolysis and by the breakdown of fatty acids through β-oxidation. Acetyl-CoA then enters the citric acid cycle, where the acetyl group is oxidized to carbon dioxide and water, and the energy ...
While botulinum toxin is generally considered safe in a clinical setting, there can be serious side effects from its use. The use of botulinum toxin A in cerebral palsy children is safe in the upper and lower limb muscles.[5][6] Most commonly, botulinum toxin can be injected into the wrong muscle group or with time spread from the injection site, causing temporary paralysis of unintended muscles. Side effects from cosmetic use generally result from unintended paralysis of facial muscles. These include partial facial paralysis, muscle weakness, and trouble swallowing. Side effects are not limited to direct paralysis however, and can also include headaches, flu-like symptoms, and allergic reactions.[41] Just as cosmetic treatments only last a number of months, paralysis side-effects can have the same durations.[citation needed] At least in some cases, these effects are reported to dissipate in the weeks after treatment.[citation needed] Bruising at the site of injection is not a side effect of the ...
... 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.[1] 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 America but is used in France, Italy and a few other countries.[2] Its use has largely been replaced by the related drug methocarbamol, which is better absorbed.[3] Mephenesin may be an NMDA receptor antagonist.[4] ...
5-HIAA is tested by 24-hour urine samples combined with an acidic additive to maintain pH below 3. Certain foods and drugs are known to interfere with the measurement. 5-HIAA levels can vary depending on other complications, including tumors, renal malfunction, and small bowel resection. Since 5-HIAA is a metabolite of serotonin, testing is most frequently performed for the diagnosis of carcinoid tumors of the enterochromaffin (Kultschitzsky) cells of the small intestine, which release large amounts of serotonin. Values greater than 25 mg per 24 hours (higher if the patient has malabsorption) are strong evidence for carcinoid. The normal range is 2 to 6 mg per 24 hours.[1] Low levels of 5-HIAA in the cerebrospinal fluid have been associated with aggressive behavior and suicide by violent means, correlating with diminished serotonin levels.[2] Elevated serotonin (hyperserotonemia) is one of the most common biological findings in autism[3] and 5-HIAA may be elevated in patients with autistic ...
... (INN,[1] codenamed ABT-089) is a drug developed by Abbott, that has nootropic and neuroprotective effects.[2][3][4] Animal studies suggested it useful for the treatment of ADHD[5] and subsequent human trials have shown ABT-089 to be effective for this application.[6] It binds with high affinity subtype-selective to the α4β2 nicotinic acetylcholine receptors and has partial agonism to the α6β2 subtype,[7][8] but not the α7 and α3β4 subtypes familiar to nicotine. It has particularly low tendency to cause side effects compared to other drugs in the class,[9][10] making it an exciting candidate for clinical development. ...
Many users report degradation of alpha-GPC when stored openly or for long periods of time. Alpha-GPC is hygroscopic and will pull moisture in from the surrounding air. This will cause the powder to turn into what appears to be a gel. Alpha-GPC with ,99% purity will undergo this process at a visible rate (seconds to minutes) and thus requires minimized exposure to the air. This hygroscopic quality can cause gel capsules not fully packed with alpha-GPC to dissolve. Proper storage methods need to be used with alpha-GPC and include removing all air from the container, double bagging with plastic bags rated for chemicals (less likely to leak air), and storing bulk/excess inside the freezer. Vacuum sealed bags are highly recommended. For people accessing alpha-GPC daily it is advisable to separate a month's supply from excess and storing the excess as best as possible. Vacuum sealing a large supply into many 1 month dividends is a method positively reported by many users. It is important to note that ...
... is a choline carbamate and a positively charged quaternary ammonium compound.[2] It is not well absorbed in the gastro-intestinal tract and does not cross the blood-brain barrier. It is usually administered topical ocular or through intraocular injection.[2] Carbachol is not easily metabolized by cholinesterase, it has a 2 to 5 minute onset of action and its duration of action is 4 to 8 hours with topical administration and 24 hours for intraocular administration. Since carbachol is poorly absorbed through topical administration, benzalkonium chloride is mixed in to promote absorption.[2]. Carbachol is a parasympathomimetic that stimulates both muscarinic and nicotinic receptors.[2] In topical ocular and intraocular administration its principal effects are miosis and increased aqueous humour outflow.[2]. In the cat and rat, carbachol is well known for its ability to induce rapid eye movement (REM) sleep when microinjected into the pontine reticular formation. Carbachol elicits this REM ...
Trimetaphan is a sulfonium compound and therefore carries a positive charge. Being charged, it cannot cross lipid cell membranes, such as those that comprise the blood-brain barrier. Due to this, trimethaphan does not have any effect on the central nervous system. The ciliary muscle of the eye functions to round the lens for accommodation and is controlled mainly by parasympathetic system input. With administration of a ganglion-blocking drug, the ciliary muscle cannot contract (cycloplegia) and the patient loses the ability to focus their eyes. Trimetaphan has a strong effect on the cardiovascular system. The size of blood vessels is primarily controlled by the sympathetic nervous system. Loss of sympathetic system input to the blood vessels causes them to get larger (vasodilation) which has the effect of lowering blood pressure. Postural hypotension is a common side effect of such drugs. Trimethaphan causes a histamine release which further lowers blood pressure. Effects on the heart include a ...
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.[22][23][24] The benzodiazepines, such as diazepam, interact with the GABAA 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.[5] Baclofen is considered to be at least as effective as diazepam in reducing spasticity, and causes much less sedation. It acts as a GABA agonist at GABAB receptors in the brain and spinal cord, resulting in hyperpolarization of neurons expressing this receptor, most likely due to increased potassium ion conductance. Baclofen also inhibits neural function presynaptically, by reducing calcium ion influx, and thereby reducing the release of excitatory ...
... is an aliphatic, sterically hindered, cyclic, tertiary amine, which is a weak base: in its protonated form it has a pKa of 11.25.[5] Pempidine is a liquid, b.p. 187-188°; d = 0.858 g/cm3.[3] Two early syntheses of this compound are those of Leonard and Hauck,[6] and Hall.[5] These are very similar in principle: Leonard and Hauck reacted phorone with ammonia, to produce 2,2,6,6-tetramethyl-4-piperidone,[7] which was then reduced by means of the Wolff-Kishner reduction to 2,2,6,6-tetramethylpiperidine; this secondary amine was then N-methylated using methyl iodide and potassium carbonate.[8] Hall's method involved reacting acetone with ammonia in the presence of calcium chloride to give 2,2,6,6-tetramethyl-4-piperidone, which was then reduced under Wolff-Kishner conditions, followed by N-methylation of the resulting 2,2,6,6-tetramethylpiperidine with methyl p-toluenesulfonate. ...
... is a gastroprokinetic agent, a drug that increases motility in the upper gastrointestinal tract. It acts directly as a serotonin 5-HT4 receptor agonist and indirectly as a parasympathomimetic. Stimulation of the serotonin receptors increases acetylcholine release in the enteric nervous system. It has been sold under the trade names Prepulsid (Janssen-Ortho) and Propulsid (in the United States). It was discovered by Janssen Pharmaceutica in 1980. In many countries, it has been either withdrawn from the market or had its indications limited due to incidences of serious cardiac side-effects. The commercial preparations of this drug are the racemic mixture of both enantiomers of the compound. The (+) enantiomer itself has the major pharmacologic effects and does not induce many of the detrimental side-effects of the mixture.[1] ...
... is an antihistamine and anticholinergic of the pyridine chemical class which was developed in the early 1950s. It was sold under the trade names Co-Pyronil and Histadyl EC.[1] It has relatively strong sedative effects, to the extent that its primary use was as a medication for insomnia rather than for its antihistamine action. Together with scopolamine, it was the main ingredient in Sominex, Nytol, and Sleep-Eze. It also provided the sedative component of Excedrin PM. All of these products were reformulated in the late 1970s when methapyrilene was demonstrated to cause liver cancer in rats when given chronically.[2] ...
There has been much debate as to whether reboxetine is more efficacious than placebo in the treatment of depression. According to a 2009 meta-analysis of 12 second-generation antidepressants, reboxetine was no more effective than placebo, and was "significantly less" effective, and less acceptable, than the other drugs in treating the acute-phase of adults with unipolar major depression.[5] The British MHRA said in September 2011 that the study had several limitations, and that "Overall the balance of benefits and risks for reboxetine remains positive in its authorised indication."[6] A UK and Europe-wide review of available efficacy and safety data has confirmed that reboxetine has benefit over placebo in its authorised indication. Efficacy was clearly shown in patients with severe or very severe depression.[6] According to a systematic review and meta-analysis by IQWiG, including unpublished data, published data on reboxetine overestimated the benefit of reboxetine versus placebo by up to 115% ...
... is an ultra-short-acting barbiturate and has been used commonly in the induction phase of general anesthesia. Its use has been largely replaced with that of propofol, but retains popularity as an induction agent for rapid sequence intubation and in obstetrics.[citation needed] Following intravenous injection, the drug rapidly reaches the brain and causes unconsciousness within 30-45 seconds. At one minute, the drug attains a peak concentration of about 60% of the total dose in the brain. Thereafter, the drug distributes to the rest of the body, and in about 5-10 minutes the concentration is low enough in the brain that consciousness returns.[citation needed]. A normal dose of sodium thiopental (usually 4-6 mg/kg) given to a pregnant woman for operative delivery (caesarian section) rapidly makes her unconscious, but the baby in her uterus remains conscious. However, larger or repeated doses can depress the baby.[6]. Sodium thiopental is not used to maintain anesthesia in ...
... ( anticholinergic agent) is a group of substances that blocks the action of the neurotransmitter acetylcholine (ACh) at synapses in the central and the peripheral nervous system, and, in broad terms, neuromuscular junction.[1][2] These agents inhibit parasympathetic nerve impulses by selectively blocking the binding of the neurotransmitter acetylcholine to its receptor in nerve cells. The nerve fibers of the parasympathetic system are responsible for the involuntary movement of smooth muscles present in the gastrointestinal tract, urinary tract, lungs, and many other parts of the body;[3] cholinergic process otherwise by enhancing ACh function.[3] In broad terms, anticholinergics are divided into two categories in accordance with their specific targets in the central, peripheral nervous system and neuromuscular junction:[3] antimuscarinic agents, and antinicotinic agents (ganglionic blockers, neuromuscular blockers).[4] In strict terms, anticholinergic only comprises ...
The usual dose of 350 mg is unlikely to engender prominent side effects other than somnolence, and mild to significant euphoria or dysphoria, but the euphoria is generally short-lived due to the fast metabolism of carisoprodol into meprobamate and other metabolites; the euphoria derived is, according to new research, most likely due to carisoprodol's inherent, potent anxiolytic effects that are far stronger than those produced by its primary metabolite, meprobamate, which is often misblamed for the drug-seeking associated with carisoprodol, as carisoprodol itself is responsible for the significantly more intense CNS effects than meprobamate alone. Carisoprodol has a unique mechanism of action, qualitatively different from that of meprobamate (Miltown). The medication is well-tolerated and without adverse effects in the majority of patients for whom it is indicated. In some patients, however, and/or early in therapy, carisoprodol can have the full spectrum of sedative side effects and can impair ...
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. ...
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 ...
Alcuronium chloride is a neuromuscular blocking (NMB) agent, alternatively referred to as a skeletal muscle relaxant. It is a ... 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- ...
Buy Alcuronium chloride - CAS Number 15180-03-7 from LGC Standards. Please login or register to view prices, check availability ...
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.. ...
4A) alcuronium. Alcuronium alone significantly suppressed basal [35S]GTPγS binding (one-way ANOVA, p , 0.0001). In the presence ... Alcuronium concentrations (−log values) for half maximum effects as estimates of the alcuronium binding affinity under the ... Ordinate, dose ratio (DR) = oxotremorine M EC50 in the presence of alcuronium divided by oxotremorine M EC50 without alcuronium ... There was no difference between the lower plateaus of the curves for alcuronium and atropine, respectively (Emax, alcuronium = ...
M alcuronium. Scatchard plots of [3H]NMS binding data obtained with and without 10(-5) M alcuronium indicated that the maximum ... The concentration of alcuronium required to diminish the binding of [3H]QNB by 50% (IC50) was 4-7 microM in the atria, ileal ... Positive cooperativity in the binding of alcuronium and N-methylscopolamine to muscarinic acetylcholine receptors.. S Tucek, J ... Positive cooperativity in the binding of alcuronium and N-methylscopolamine to muscarinic acetylcholine receptors.. S Tucek, J ...
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 ...
Alcuronium chloride [USAN:INN:BAN:JAN] - Similar structures search, synonyms, formulas, resource links, and other chemical ... Substance Name: Alcuronium chloride [USAN:INN:BAN:JAN]. RN: 15180-03-7. UNII: 490DW6501Y. InChIKey: CPYGBGOXCJJJGC-GKLGUMFISA-L ...
ALCURONIUM. Alcuronium chloride is a drug that belongs to a class of medicines known as benzylisoquinolinium competitive ... Alcuronium chloride can give rise to side effects such as fast heartbeat (tachycardia) and decreased blood pressure ( ... Alcuronium chloride is used in endotracheal intubation and as a muscle relaxant in general anesthesia. ...
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 ...
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.
Alcuronium *Alphaxalone Alphadolone Alprazolam Aluminium Preparations Amidopyrine Aminoglutethimide Aminophylline Amiodarone * ...
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Coleman AJ, Downing JW, Leary WP, Moyes DG (1972). "The immediate cardiovascular effects of pancuronium, alcuronium and ...
Alcuronium. The therapeutic efficacy of Alcuronium can be increased when used in combination with Carindacillin. ...
Alcuronium. The therapeutic efficacy of Polyethylene glycol can be decreased when used in combination with Alcuronium. ...
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.
d-tuburcurarine, mivacurium, metocurine, atracurium, alcuronium. Term. aminosteroid nondepolarizing neuromuscular blockers. ...
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Merck & Co., Inc., Kenilworth, NJ, USA is a global healthcare leader working to help the world be well. From developing new therapies that treat and prevent disease to helping people in need, we are committed to improving health and well-being around the world. The Merck Veterinary Manual was first published in 1955 as a service to the community. The legacy of this great resource continues as the Merck Veterinary Manual in the US and Canada and the MSD Manual outside of North America.. ...
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A clinical comparison of pancuronium with tubocurarine and alcuronium in major cardiothoracic surgery. ...
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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  • Alcuronium Chloride (PH: BP 2011, Ph. (drugs.com)
  • Alcuronium chloride is a neuromuscular blocking (NMB) agent, alternatively referred to as a skeletal muscle relaxant. (wikipedia.org)
  • Alcuronium chloride is a drug that belongs to a class of medicines known as benzylisoquinolinium competitive neuromuscular blockers. (watsonshealth.com.ph)
  • Alcuronium chloride is used in endotracheal intubation and as a muscle relaxant in general anesthesia. (watsonshealth.com.ph)
  • Alcuronium chloride can give rise to side effects such as fast heartbeat (tachycardia) and decreased blood pressure (hypotension). (watsonshealth.com.ph)
  • 6) In European kestrels (Falco tinnunculus), mydriasis was inconsistent with topical pancuronium bromide, and although effectively achieved with topical alcuronium chloride, birds developed temporary inferior eyelid paralysis (5/8 birds) and neck and limb paralysis (1/8 birds) with topical alcuronium chloride. (thefreelibrary.com)
  • Then 45 mg alcuronium chloride (Alloferin) or 18 mg pancuronium bromide (Pavulon) is injected. (conservativeunderground.com)
  • Muscle relaxants like alcuronium, pancuronium and atracurium associated with or without atropine prolong significantly the QT interval. (uptodate.com)
  • The replacement of both the N-methyl groups with N-allyl moieties yielded N,N-diallyl-bis-nortoxiferine, now recognized as alcuronium (and at one time marketed as the proprietary agent called Alloferin). (wikipedia.org)
  • The pharmacological action of alcuronium is readily reversed by neostigmine, and it produced little histamine release. (wikipedia.org)
  • The effect of halothane on the action of alcuronium on neuromuscular transmission was studied in the intact dog. (uzh.ch)
  • investigated the effects of alcuronium, brucine, and structurally related compounds on the equilibrium binding of 12 agonists in cloned M 1 -M 4 receptors. (aspetjournals.org)
  • In contrast to [3H] NMS, the effects of alcuronium on the binding of [3H]QNB were only inhibitory. (aspetjournals.org)
  • Drugs in this group include tubocurarine, gallamine, pancuronium, alcuronium and vecuronium ( Table 4.1 ). (veteriankey.com)
  • Inclusion of the allylic functions presented an enhanced potential area of biotransformation, and thus alcuronium is observed to have a much shorter duration of neuromuscular blocking action than its parent C-toxiferine I. It also has a more rapid onset of action, and is ~1.5 times as potent as tubocurarine. (wikipedia.org)
  • In support of this hypothesis, pilocarpine acted as a competitive antagonist against oxotremorine M in the presence of 10 μM alcuronium. (aspetjournals.org)
  • The major disadvantage of alcuronium is that it elicits a vagolytic effect produced by a selective atropine-like blockade of cardiac muscarinic receptors. (wikipedia.org)
  • 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. (aspetjournals.org)
  • Positive cooperativity in the binding of alcuronium and N-methylscopolamine to muscarinic acetylcholine receptors. (aspetjournals.org)
  • The rates of [3H]NMS association to and dissociation from muscarinic binding sites in the atria were diminished by 10(-5) M alcuronium. (aspetjournals.org)
  • The results suggest that the binding of low concentrations of alcuronium to muscarinic receptors in the heart, ileal smooth muscle, and cerebellum allosterically increases the affinity of muscarinic receptors towards [3H]NMS, although not [3H]QNB. (aspetjournals.org)
  • At high concentrations, alcuronium inhibits the binding of muscarinic ligands, presumably by competition for the classical muscarinic binding site. (aspetjournals.org)
  • Positive cooperativity induced by alcuronium appears to be specific for the m2 (cardiac) subtype of muscarinic receptors. (aspetjournals.org)
  • 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. (aspetjournals.org)
  • 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. (aspetjournals.org)
  • In conclusion, alcuronium converted the agonist pilocarpine into an antagonist-a novel type of functional allosteric interaction. (aspetjournals.org)
  • Among the allosteric agents, alcuronium had, by far, the highest affinity for M 2 receptors. (aspetjournals.org)
  • This can be the case for the propenyl ammonium groups present in rocuronium and alcuronium 4, 9 . (worldallergy.org)
  • 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 (p K A, Alc = 5.54). (aspetjournals.org)
  • If pilocarpine remained receptor bound in the presence of alcuronium, this indicates that pilocarpine can no longer act as an agonist. (aspetjournals.org)
  • Alcuronium suppressed pilocarpine-induced stimulation of [ 35 S]GTPγS binding (pIC 50, Alc = 5.47) without shift in EC 50 , whereas it competitively shifted the response to oxotremorine M (p K A, Alc = 5.97). (aspetjournals.org)
  • When pilocarpine was bound to the M 2 receptors, the affinity of alcuronium was even somewhat increased. (aspetjournals.org)
  • means a 2.7-fold higher affinity of alcuronium for pilocarpine-occupied M 2 receptors compared with free receptors. (aspetjournals.org)
  • Alcuronium (chlorure d') (PH: Ph. (drugs.com)
  • The concentration of alcuronium required to diminish the binding of [3H]QNB by 50% (IC50) was 4-7 microM in the atria, ileal smooth muscle, and the cerebellum, 140 microM in the brain cortex, and 1200 microM in the parotid gland. (aspetjournals.org)
  • The binding of [3H]NMS was inhibited at 10(-3) M and higher concentrations of alcuronium. (aspetjournals.org)
  • Scatchard plots of [3H]NMS binding data obtained with and without 10(-5) M alcuronium indicated that the maximum number of binding sites was not altered by the drug, whereas the apparent Kd for [3H]NMS was diminished. (aspetjournals.org)
  • Inhaltsstoffe enthalten können, können die Preise the impurity profile of alcuronium by means of capillary electrophoresis. (clcblog.org)