Open AccessAcetylcholine Receptors Do Not Mediate the Immobilization Produced by Inhaled Anesthetics
Author(s) -
Edmond I. Eger,
Yi Zhang,
Michael J. Laster,
Pamela Flood,
Joan J. Kendig,
James M. Sonner
Publication year - 2002
Publication title -
anesthesia and analgesia/anesthesia and analgesia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.404
H-Index - 201
eISSN - 1526-7598
pISSN - 0003-2999
DOI - 10.1097/00000539-200206000-00023
Subject(s) - mecamylamine , muscarinic acetylcholine receptor , atropine , acetylcholine , pharmacology , medicine , isoflurane , nicotinic agonist , acetylcholine receptor , anesthesia , stimulation , muscarinic acetylcholine receptor m2 , receptor , endocrinology
Acetylcholine receptors transmit excitatory impulses, are broadly distributed throughout the central nervous system, and are particularly sensitive to the depressant effects of inhaled anesthetics. Thus these receptors are potential mediators of the immobility produced by inhaled anesthetics. We tested this potential in rats by giving intraperitoneal atropine, scopolamine, and mecamylamine to block muscarinic (atropine and scopolamine) and neuronal nicotinic (mecamylamine) acetylcholine receptors. Block with scopolamine (up to 100 mg/kg), atropine (10 mg/kg), mecamylamine (up to 4 mg/kg), or atropine (10 mg/kg) plus mecamylamine (up to 4 mg/kg) did not significantly decrease the isoflurane concentration required to suppress movement to noxious stimulation (minimum alveolar anesthetic concentration). We also gave atropine intrathecally, finding that the infusions that did not cause permanent paralysis produced slight or no decreases in the minimum alveolar anesthetic concentration. We conclude that acetylcholine receptors do not seem to play a role as mediators of immobilization by inhaled anesthetics.