メタコリン、塩化メタコリン
WordNet
- any compound containing a chlorine atom
- any salt of hydrochloric acid (containing the chloride ion)
- parasympathomimetic drug (trademark Mecholyl) that stimulates secretions and smooth muscle activity (同)Mecholyl
PrepTutorEJDIC
- 塩化物
Wikipedia preview
出典(authority):フリー百科事典『ウィキペディア(Wikipedia)』「2013/05/08 17:59:23」(JST)
[Wiki en表示]
Methacholine
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Systematic (IUPAC) name |
2-(Acetyloxy)-N,N,N-trimethylpropan-1-aminium |
Clinical data |
AHFS/Drugs.com |
International Drug Names |
Pregnancy cat. |
? |
Legal status |
? |
Identifiers |
CAS number |
55-92-5 N
62-51-1 (chloride) |
ATC code |
None |
PubChem |
CID 6114 |
DrugBank |
DB06709 |
ChemSpider |
5888 Y |
UNII |
03V657ZD3V Y |
KEGG |
D04970 Y |
ChEBI |
CHEBI:50142 Y |
ChEMBL |
CHEMBL978 N |
Chemical data |
Formula |
C8H18NO2+ |
Mol. mass |
160.234 g/mol |
SMILES
- [Cl-].O=C(OC(C)C[N+](C)(C)C)C
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InChI
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InChI=1S/C8H18NO2.ClH/c1-7(11-8(2)10)6-9(3,4)5;/h7H,6H2,1-5H3;1H/q+1;/p-1 Y
Key:JHPHVAVFUYTVCL-UHFFFAOYSA-M Y
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N (what is this?) (verify)
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Methacholine (Provocholine) is a synthetic choline ester that acts as a non-selective muscarinic receptor agonist in the parasympathetic nervous system.
Contents
- 1 Uses
- 2 Pharmacology
- 3 Contraindications
- 4 References
- 5 External links
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Uses [edit]
Methacholine is primarily used to diagnose bronchial hyperreactivity,[1] which is the hallmark of asthma and also occurs in chronic obstructive pulmonary disease. This is accomplished through the bronchial challenge test, or methacholine challenge, in which a subject inhales aerosolized methacholine, leading to bronchoconstriction. Other therapeutic uses are limited by its adverse cardiovascular effects, such as bradycardia and hypotension, which arise from its function as a cholinomimetic.
Pharmacology [edit]
It is highly active at all of the muscarinic receptors, but has little effect on the nicotinic receptors. Methacholine has a charged quaternary amine structure, rendering it insoluble to lipid cell membranes. Clinically, this means that it will not cross the blood–brain barrier and has poor absorption from the gastrointestinal tract. It is broken down at a relatively slow rate within the body, due to its resistance to acetylcholinesterases.
Methacholine has a β-methyl group which provides selectivity towards M-type receptors as compared to N-type receptors. The quaternary ammonium group is essential for activity. The ester however makes it susceptible to the enzyme acetylcholine esterase.[2]
Contraindications [edit]
Use of methacholine is contraindicated in patients with recent heart attack or stroke, uncontrolled hypertension, known severe airway disease, or an aortic aneurysm. It may be used with caution by nursing or pregnant mothers and patients taking certain medications for myasthenia gravis.[3]
References [edit]
- ^ Birnbaum S, Barreiro TJ (June 2007). "Methacholine challenge testing: identifying its diagnostic role, testing, coding, and reimbursement". Chest 131 (6): 1932–5. doi:10.1378/chest.06-1385. PMID 17565027.
- ^ Medicinal Chemistry of Adrenergics and Cholinergics
- ^ http://ajrccm.atsjournals.org/cgi/content/full/161/1/309
External links [edit]
Cholinergics
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Receptor ligands
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mAChR
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- Agonists: 77-LH-28-1
- AC-42
- AC-260,584
- Aceclidine
- Acetylcholine
- AF30
- AF150(S)
- AF267B
- AFDX-384
- Alvameline
- AQRA-741
- Arecoline
- Bethanechol
- Butyrylcholine
- Carbachol
- CDD-0034
- CDD-0078
- CDD-0097
- CDD-0098
- CDD-0102
- Cevimeline
- Choline
- cis-Dioxolane
- Ethoxysebacylcholine
- LY-593,039
- L-689,660
- LY-2,033,298
- McNA343
- Methacholine
- Milameline
- Muscarine
- NGX-267
- Ocvimeline
- Oxotremorine
- PD-151,832
- Pilocarpine
- RS86
- Sabcomeline
- SDZ 210-086
- Sebacylcholine
- Suberylcholine
- Talsaclidine
- Tazomeline
- Thiopilocarpine
- Vedaclidine
- VU-0029767
- VU-0090157
- VU-0152099
- VU-0152100
- VU-0238429
- WAY-132,983
- Xanomeline
- YM-796
Antagonists: 3-Quinuclidinyl Benzilate
- 4-DAMP
- Aclidinium Bromide
- Anisodamine
- Anisodine
- Atropine
- Atropine Methonitrate
- Benactyzine
- Benzatropine/Benztropine
- Benzydamine
- BIBN 99
- Biperiden
- Bornaprine
- CAR-226,086
- CAR-301,060
- CAR-302,196
- CAR-302,282
- CAR-302,368
- CAR-302,537
- CAR-302,668
- CS-27349
- Cyclobenzaprine
- Cyclopentolate
- Darifenacin
- DAU-5884
- Dimethindene
- Dexetimide
- DIBD
- Dicyclomine/Dicycloverine
- Ditran
- EA-3167
- EA-3443
- EA-3580
- EA-3834
- Etanautine
- Etybenzatropine/Ethylbenztropine
- Flavoxate
- Himbacine
- HL-031,120
- Ipratropium bromide
- J-104,129
- Hyoscyamine
- Mamba Toxin 3
- Mamba Toxin 7
- Mazaticol
- Mebeverine
- Methoctramine
- Metixene
- N-Ethyl-3-Piperidyl Benzilate
- N-Methyl-3-Piperidyl Benzilate
- Orphenadrine
- Otenzepad
- Oxybutynin
- PBID
- PD-102,807
- PD-0298029
- Phenglutarimide
- Phenyltoloxamine
- Pirenzepine
- Piroheptine
- Procyclidine
- Profenamine
- RU-47,213
- SCH-57,790
- SCH-72,788
- SCH-217,443
- Scopolamine/Hyoscine
- Solifenacin
- Telenzepine
- Tiotropium bromide
- Tolterodine
- Trihexyphenidyl
- Tripitamine
- Tropatepine
- Tropicamide
- WIN-2299
- Xanomeline
- Zamifenacin; Others: 1st Generation Antihistamines (Brompheniramine
- chlorphenamine
- cyproheptadine
- dimenhydrinate
- diphenhydramine
- doxylamine
- mepyramine/pyrilamine
- phenindamine
- pheniramine
- tripelennamine
- triprolidine, etc)
- Tricyclic Antidepressants (Amitriptyline
- doxepin
- trimipramine, etc)
- Tetracyclic Antidepressants (Amoxapine
- maprotiline, etc)
- Typical Antipsychotics (Chlorpromazine
- thioridazine, etc)
- Atypical Antipsychotics (Clozapine
- olanzapine, etc.)
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nAChR
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- Agonists: 5-HIAA
- A-84,543
- A-366,833
- A-582,941
- A-867,744
- ABT-202
- ABT-418
- ABT-560
- ABT-894
- Acetylcholine
- Altinicline
- Anabasine
- Anatoxin-a
- AR-R17779
- Butinoline
- Butyrylcholine
- Carbachol
- Choline
- Cotinine
- Cytisine
- Decamethonium
- Desformylflustrabromine
- Dianicline
- Dimethylphenylpiperazinium
- Epibatidine
- Epiboxidine
- Ethanol
- Ethoxysebacylcholine
- EVP-4473
- EVP-6124
- Galantamine
- GTS-21
- Ispronicline
- Lobeline
- MEM-63,908/RG-3487
- Nicotine
- NS-1738
- PHA-543,613
- PHA-709,829
- PNU-120,596
- PNU-282,987
- Pozanicline
- Rivanicline
- RJR-2429
- Sazetidine A
- Sebacylcholine
- SIB-1508Y
- SIB-1553A
- SSR-180,711
- Suberylcholine
- Suxamethonium/Succinylcholine
- TC-1698
- TC-1734
- TC-1827
- TC-2216
- TC-5214
- TC-5619
- TC-6683
- Tebanicline
- Tropisetron
- UB-165
- Varenicline
- WAY-317,538
- XY-4083
Antagonists: 18-Methoxycoronaridine
- α-Bungarotoxin
- α-Conotoxin
- Alcuronium
- Amantadine
- Anatruxonium
- Atracurium
- Bupropion
- Chandonium
- Chlorisondamine
- Cisatracurium
- Coclaurine
- Coronaridine
- Dacuronium
- Decamethonium
- Dextromethorphan
- Dextropropoxyphene
- Dextrorphan
- Diadonium
- DHβE
- Dimethyltubocurarine/Metocurine
- Dipyrandium
- Dizocilpine/MK-801
- Doxacurium
- Duador
- Esketamine
- Fazadinium
- Gallamine
- Hexafluronium
- Hexamethonium/Benzohexonium
- Ibogaine
- Isoflurane
- Ketamine
- Kynurenic acid
- Laudexium/Laudolissin
- Levacetylmethadol
- Malouetine
- Mecamylamine
- Memantine
- Methadone (Levomethadone)
- Methorphan/Racemethorphan
- Methyllycaconitine
- Metocurine
- Mivacurium
- Morphanol/Racemorphan
- Neramexane
- Nitrous Oxide
- Pancuronium
- Pempidine
- Pentamine
- Pentolinium
- Phencyclidine
- Pipecuronium
- Radafaxine
- Rapacuronium
- Rocuronium
- Surugatoxin
- Thiocolchicoside
- Toxiferine
- Trimethaphan
- Tropeinium
- Tubocurarine
- Vecuronium
- Xenon
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Reuptake inhibitors
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Plasmalemmal
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CHT Inhibitors
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- Hemicholinium-3/Hemicholine
- Triethylcholine
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Vesicular
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Enzyme inhibitors
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Anabolism
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ChAT inhibitors
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- 1-(-Benzoylethyl)pyridinium
- 2-(α-Naphthoyl)ethyltrimethylammonium
- 3-Chloro-4-stillbazole
- 4-(1-Naphthylvinyl)pyridine
- Acetylseco hemicholinium-3
- Acryloylcholine
- AF64A
- B115
- BETA
- CM-54,903
- N,N-Dimethylaminoethylacrylate
- N,N-Dimethylaminoethylchloroacetate
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Catabolism
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AChE inhibitors
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BChE inhibitors
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- Cymserine * Many of the acetylcholinesterase inhibitors listed above act as butyrylcholinesterase inhibitors.
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Others
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Precursors
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- Choline (Lecithin)
- Citicoline
- Cyprodenate
- Dimethylethanolamine
- Glycerophosphocholine
- Meclofenoxate/Centrophenoxine
- Phosphatidylcholine
- Phosphatidylethanolamine
- Phosphorylcholine
- Pirisudanol
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Cofactors
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- Acetic acid
- Acetylcarnitine
- Acetyl-coA
- Vitamin B5 (Pantethine
- Pantetheine
- Panthenol)
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Others
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- Acetylcholine releasing agents: α-Latrotoxin
- β-Bungarotoxin; Acetylcholine release inhibitors: Botulinum toxin (Botox); Acetylcholinesterase reactivators: Asoxime
- Obidoxime
- Pralidoxime
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UpToDate Contents
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English Journal
- Pharmacological enhancement of leg and muscle microvascular blood flow does not augment anabolic responses in skeletal muscle of young men under fed conditions.
- Phillips BE1, Atherton PJ, Varadhan K, Wilkinson DJ, Limb M, Selby AL, Rennie MJ, Smith K, Williams JP.Author information 1Division of Medical Science and Graduate Entry Medicine, University of Nottingham, Royal Derby Hospital, Derby, United Kingdom; and.AbstractSkeletal muscle anabolism associated with postprandial plasma aminoacidemia and insulinemia is contingent upon amino acids (AA) and insulin crossing the microcirculation-myocyte interface. In this study, we hypothesized that increasing muscle microvascular blood volume (flow) would enhance fed-state anabolic responses in muscle protein turnover. We studied 10 young men (23.2 ± 2.1 yr) under postabsorptive and fed [iv Glamin (∼10 g AA), glucose ∼7.5 mmol/l] conditions. Methacholine was infused into the femoral artery of one leg to determine, via bilateral comparison, the effects of feeding alone vs. feeding plus pharmacological vasodilation. We measured leg blood flow (LBF; femoral artery) by Doppler ultrasound, muscle microvascular blood volume (MBV) by contrast-enhanced ultrasound (CEUS), muscle protein synthesis (MPS) and breakdown (MPB; a-v balance modeling), and net protein balance (NPB) using [1,2-(13)C2]leucine and [(2)H5]phenylalanine tracers via gas chromatography-mass spectrometry (GC-MS). Indexes of anabolic signaling/endothelial activation (e.g., Akt/mTORC1/NOS) were assessed using immunoblotting techniques. Under fed conditions, LBF (+12 ± 5%, P < 0.05), MBV (+25 ± 10%, P < 0.05), and MPS (+129 ± 33%, P < 0.05) increased. Infusion of methacholine further enhanced LBF (+126 ± 12%, P < 0.05) and MBV (+79 ± 30%, P < 0.05). Despite these radically different blood flow conditions, neither increases in MPS in response to feeding (0.04 ± 0.004 vs. 0.08 ± 0.01%/h, P < 0.05) nor improvements in NPB (-4.4 ± 2.4 vs. 16.4 ± 5.7 nmol Phe·100 ml leg(-1)·min(-1), P < 0.05) were affected by methacholine infusion (MPS 0.07 ± 0.01%/h; NPB 24.0 ± 7.7 nmol Phe·100 ml leg(-1)·min(-1)), whereas MPB was unaltered by either feeding or infusion of methacholine. Thus, enhancing LBF/MBV above that occurring naturally with feeding alone does not improve muscle anabolism.
- American journal of physiology. Endocrinology and metabolism.Am J Physiol Endocrinol Metab.2014 Jan 15;306(2):E168-76. doi: 10.1152/ajpendo.00440.2013. Epub 2013 Nov 26.
- Skeletal muscle anabolism associated with postprandial plasma aminoacidemia and insulinemia is contingent upon amino acids (AA) and insulin crossing the microcirculation-myocyte interface. In this study, we hypothesized that increasing muscle microvascular blood volume (flow) would enhance fed-state
- PMID 24280127
- Deletion of airway cilia results in noninflammatory bronchiectasis and hyperreactive airways.
- Gilley SK1, Stenbit AE, Pasek RC, Sas KM, Steele SL, Amria M, Bunni MA, Estell KP, Schwiebert LM, Flume P, Gooz M, Haycraft CJ, Yoder BK, Miller C, Pavlik JA, Turner GA, Sisson JH, Bell PD.Author information 170 President St, DDB520, MUSC, Charleston, SC 29425. Bellpd@musc.edu.AbstractThe mechanisms for the development of bronchiectasis and airway hyperreactivity have not been fully elucidated. Although genetic, acquired diseases and environmental influences may play a role, it is also possible that motile cilia can influence this disease process. We hypothesized that deletion of a key intraflagellar transport molecule, IFT88, in mature mice causes loss of cilia, resulting in airway remodeling. Airway cilia were deleted by knockout of IFT88, and airway remodeling and pulmonary function were evaluated. In IFT88(-) mice there was a substantial loss of airway cilia on respiratory epithelium. Three months after the deletion of cilia, there was clear evidence for bronchial remodeling that was not associated with inflammation or apparent defects in mucus clearance. There was evidence for airway epithelial cell hypertrophy and hyperplasia. IFT88(-) mice exhibited increased airway reactivity to a methacholine challenge and decreased ciliary beat frequency in the few remaining cells that possessed cilia. With deletion of respiratory cilia there was a marked increase in the number of club cells as seen by scanning electron microscopy. We suggest that airway remodeling may be exacerbated by the presence of club cells, since these cells are involved in airway repair. Club cells may be prevented from differentiating into respiratory epithelial cells because of a lack of IFT88 protein that is necessary to form a single nonmotile cilium. This monocilium is a prerequisite for these progenitor cells to transition into respiratory epithelial cells. In conclusion, motile cilia may play an important role in controlling airway structure and function.
- American journal of physiology. Lung cellular and molecular physiology.Am J Physiol Lung Cell Mol Physiol.2014 Jan;306(2):L162-9. doi: 10.1152/ajplung.00095.2013. Epub 2013 Nov 8.
- The mechanisms for the development of bronchiectasis and airway hyperreactivity have not been fully elucidated. Although genetic, acquired diseases and environmental influences may play a role, it is also possible that motile cilia can influence this disease process. We hypothesized that deletion of
- PMID 24213915
- Airway hyper-responsiveness in lipopolysaccharide-challenged common marmosets (Callithrix jacchus).
- Curths C1, Wichmann J, Dunker S, Windt H, Hoymann HG, Lauenstein HD, Hohlfeld J, Becker T, Kaup FJ, Braun A, Knauf S.Author information 1‡Pathology Unit, German Primate Center, Leibniz-Institute, Kellnerweg 4, 37077 Göttingen, Germany.AbstractAnimal models with a high predictive value for human trials are needed to develop novel human-specific therapeutics for respiratory diseases. The aim of the present study was to examine lung-function parameters in marmoset monkeys (Callithrix jacchus) that can be used to detect pharmacologically or provocation-induced AHR (airway hyper-responsiveness). Therefore a custom-made lung-function device that allows application of defined aerosol doses during measurement was developed. It was hypothesized that LPS (lipopolysaccharide)-challenged marmosets show AHR compared with non-challenged healthy subjects. Invasive plethysmography was performed in 12 anaesthetized orotracheally intubated and spontaneously breathing marmosets. Pulmonary data of R(L) (lung resistance), C(dyn) (dynamic compliance), EF50 (mid-expiratory flow), P(oes) (oesophageal pressure), MV (minute volume), respiratory frequency (f) and V(T) (tidal volume) were collected. Measurements were conducted under baseline conditions and under MCh (methacholine)-induced bronchoconstriction. The measurement was repeated with the same group of animals after induction of an acute lung inflammation by intratracheal application of LPS. PDs (provocative doses) of MCh to achieve a certain increase in RL were significantly lower after LPS administration. AHR was demonstrated in the LPS treated compared with the naïve animals. The recorded lung-function data provide ground for pre-clinical efficacy and safety testing of anti-inflammatory substances in the common marmoset, a new translational NHP (non-human primate) model for LPS-induced lung inflammation.
- Clinical science (London, England : 1979).Clin Sci (Lond).2014 Jan;126(2):155-62. doi: 10.1042/CS20130101.
- Animal models with a high predictive value for human trials are needed to develop novel human-specific therapeutics for respiratory diseases. The aim of the present study was to examine lung-function parameters in marmoset monkeys (Callithrix jacchus) that can be used to detect pharmacologically or
- PMID 23879175
Japanese Journal
- 気管支喘息と慢性気管支炎における末梢気道障害と気道過敏性に関する研究
- 星野 重幸
- アレルギー 35(11), 1079-1087, 1986-11-30
- 気管支喘息および慢性気管支炎における末梢気道検査も含めた気道閉塞の因子とアストグラフによる塩化メタコリン吸入試験の諸指標の関係について健常者のそれと比較検討して, 以下の結果を得た.1)bronchial sensitivity(Dmin)は, 気管支喘息, 慢性気管支炎, 健常者の順に低値であったが, bronchial reactivity(SGrs/Grsc)は, 気管支喘息と慢性気管支炎お …
- NAID 110002414817
- SARTストレスマウスにおける異常心電図とMethacholine不整脈の発現ならびにOxprenololなどβ遮断薬の作用
- 秦 多恵子,喜多 富太郎,伊藤 栄次,原田 典子
- 日本薬理学雑誌 83(5), 413-424, 1984
- … 投与したところ,いずれの不整脈も正常マウスより低頻度に出現した.次にmethacholine chloride 300μg/kg,i.v.により不整脈を惹起させ,出現頻度を求めたところ,SARTマウスでは期外収縮,房室ブロックおよび洞房ブロックの出現が正常マウスのそれより有意に高頻度であった,次にSARTマウスにおけるmethacholine不整脈発現に及ぼすoxprenolol,propranololおよびcarteololなどの阻止効果を調べ …
- NAID 130000761007
Related Links
- Provocholine (Methacholine Chloride) manufactured by Methapharm is indicated for the diagnosis of bronchial airway hyperreactivity in subjects who do not have clinically apparent asthma. www.provocholine.com ... WARNING ...
- These are trials that mention methacholine chloride and are related to either pharmacogenetics or pharmacogenomics. Common Searches Search PubMed Search Medline Plus Search PubChem Search CTD Sources forDrugBank. ...
Related Pictures
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★リンクテーブル★
[★]
- 英
- methacholine
- 同
- メサコリン
- 化
- 塩化メタコリン, methacholine chloride、臭化メタコリン, methacholine bromide
- 関
[show details]
[★]
塩素イオン