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Cholinesterases and the resistance of the mouse diaphragm to the effect of tubocurarine
- Source :
- Anesthesiology, Anesthesiology, Lippincott, Williams & Wilkins, 2005, 103 (4), pp.788-795
- Publication Year :
- 2005
- Publisher :
- HAL CCSD, 2005.
-
Abstract
- Background The diaphragm is resistant to competitive neuromuscular blocking agents. Because of the competitive mechanism of action of tubocurarine, the rate of hydrolysis of acetylcholine at the neuromuscular junction may modulate its neuromuscular blocking effect. The authors compared the neuromuscular blocking effect of tubocurarine on isolated diaphragm and extensor digitorum longus (EDL) muscles and quantified the acetylcholinesterase activity in hetero-oligomers. Methods Adult Swiss-Webster and collagen Q-deficient (ColQ) mice were used. The blocking effect of tubocurarine on nerve-evoked muscle twitches was determined in isolated diaphragm and EDL muscles, after inhibition of acetylcholinesterase by fasciculin-1, butyrylcholinesterase by tetraisopropylpyro-phosphoramide, or both acetylcholinesterase and butyrylcholinesterase by neostigmine, and in acetylcholinesterase-deficient ColQ muscles. The different acetylcholinesterase oligomers extracted from diaphragm and EDL muscles were quantified in sucrose gradient. Results The EC50 for tubocurarine to decrease the nerve-evoked twitch response was four times higher in the diaphragm than in the EDL. The activity of the different acetylcholinesterase oligomers was lower in the diaphragm as compared with the EDL. Inhibition of acetylcholinesterase by antagonists resulted in an increased dose of tubocurarine but an unchanged resistance ratio between the diaphragm and the EDL. A similar diaphragmatic resistance was found in ColQ muscles. Conclusion The current study indicates that, despite differences in acetylcholinesterase activity between the diaphragm and EDL, the diaphragmatic resistance to tubocurarine cannot be explained by the different rate of acetylcholine hydrolysis in the synaptic cleft.
- Subjects :
- MESH : Neuromuscular Nondepolarizing Agents
Drug Resistance
Muscle Proteins
Tubocurarine
MESH : Dose-Response Relationship, Drug
Receptors, Nicotinic
MESH: Dose-Response Relationship, Drug
chemistry.chemical_compound
Mice
0302 clinical medicine
030202 anesthesiology
MESH: Collagen
COLQ
Medicine
MESH: Animals
MESH : Tubocurarine
MESH : Muscle Proteins
biology
musculoskeletal, neural, and ocular physiology
Neuromuscular Blocking Agents
musculoskeletal system
Acetylcholinesterase
Diaphragm (structural system)
medicine.anatomical_structure
Biochemistry
MESH: Receptors, Nicotinic
MESH: Drug Resistance
[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]
Collagen
tissues
Acetylcholine
medicine.drug
medicine.medical_specialty
Synaptic cleft
Diaphragm
Neuromuscular Junction
In Vitro Techniques
Neuromuscular junction
MESH : Acetylcholinesterase
03 medical and health sciences
MESH: Muscle Proteins
Internal medicine
MESH : Mice
Animals
MESH: Tubocurarine
[SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]
MESH: Mice
Cholinesterase
MESH : Drug Resistance
MESH : Receptors, Nicotinic
Dose-Response Relationship, Drug
business.industry
MESH: Acetylcholinesterase
Anesthesiology and Pain Medicine
Endocrinology
chemistry
MESH: Diaphragm
MESH : Collagen
biology.protein
MESH : Neuromuscular Junction
MESH : Animals
MESH: Neuromuscular Junction
MESH : Diaphragm
business
MESH: Neuromuscular Nondepolarizing Agents
030217 neurology & neurosurgery
Neuromuscular Nondepolarizing Agents
Subjects
Details
- Language :
- English
- ISSN :
- 00033022
- Database :
- OpenAIRE
- Journal :
- Anesthesiology, Anesthesiology, Lippincott, Williams & Wilkins, 2005, 103 (4), pp.788-795
- Accession number :
- edsair.doi.dedup.....71baf9e9d63b86dee2e42c9572d94730