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ANESTHETIC PHARMACOLOGY

Blockade of Acetylcholine Receptors Does Not Change the Dose of Etomidate Required to Produce Immobility in Rats

Yi Zhang, MD, Michael J. Laster, DVM^*, Edmond I. Eger, II, MD^*, Manohar Sharma, PhD^*, and James M. Sonner, MD^*

From the *Department of Anesthesia and Perioperative Care, University of California, San Francisco, California, and the Department of Anesthesiology, Fuwai Hospital and Cardiovascular Institute, Beijing, China.

Address correspondence and reprint requests to Edmond Eger, II, MD, Department of Anesthesia, S-455, University of California, San Francisco, CA 94143-0464. Address e-mail to egere{at}anesthesia.ucsf.edu.

BACKGROUND: Administration of drugs blocking muscarinic plus neuronal nicotinic acetylcholine receptors (e.g., atropine and mecamylamine) does not affect the MAC of isoflurane. Although this implies that acetylcholine receptors do not mediate the immobility produced by inhaled anesthetics, another interpretation is possible. Sub-MAC concentrations of isoflurane alone profoundly block acetylcholine receptors, allowing for the possibility that atropine and mecamylamine have no effect because the receptors already are blocked.

METHODS: In the present study, we indirectly tested this possibility by measuring the capacity of acetylcholine receptor blockade to decrease the anesthetic requirement for etomidate, an anesthetic thought to act solely by enhancing the effect of -aminobutyric acid on -aminobutyric acid_A receptors.

RESULTS: Administration of 10 mg/kg atropine plus 5 mg/kg mecamylamine did not change the infusion rate of etomidate, or the blood or brain concentrations of etomidate required to produce immobility in rats.

CONCLUSION: Acetylcholine receptors do not mediate the capacity of anesthetics to produce immobility in the face of noxious stimulation.

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