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Correlating the clinical actions and molecular mechanisms of general anesthetics

Solt, Kena,b; Forman, Stuart Aa,b

Current Opinion in Anaesthesiology: August 2007 - Volume 20 - Issue 4 - p 300–306
doi: 10.1097/ACO.0b013e32816678a5
Drugs in anaesthesia

Purpose of review To summarize recent in-vitro and in-vivo research on molecular mechanisms of general anesthetics' actions.

Recent findings Classes of general anesthetics with distinct clinical profiles appear to induce amnesia, hypnosis, and immobility via different molecular targets. Propofol, etomidate, and barbiturates produce profound amnesia and hypnosis, but weak immobility, by enhancing the activity of specific gamma-aminobutyric acid typeA receptors. In contrast, nitrous oxide, xenon, and ketamine produce analgesia, but weak hypnosis and amnesia, by inhibiting glutamate and nicotinic receptors and activating potassium ‘leak’ channels such as TREK-1. Volatile halogenated anesthetics show little selectivity for molecular targets. They act on all the channels mentioned above, and other targets such as glycine receptors and mediators of neurotransmitter release.

Summary Several clinically distinct ‘anesthetic states’ are induced by different classes of drugs acting on neuronal circuits via different molecular targets. Understanding the mechanisms underlying the therapeutic and toxic actions of general anesthetics helps us reframe the ‘art’ of anesthesia into more of a ‘science’. These studies also enhance efforts to develop new drugs with improved clinical utility.

aDepartment of Anesthesia and Critical Care, Massachusetts General Hospital, Boston, USA

bDepartment of Anesthesia, Harvard Medical School, Boston, USA

Correspondence to Stuart A. Forman, MD, PhD, Department of Anesthesia and Critical Care, Massachusetts General Hospital, 55 Fruit Street, Gray 444, Boston, MA 02114, USA Tel: +1 617 724 5156; fax: +1 617 724 8644; e-mail:

© 2007 Lippincott Williams & Wilkins, Inc.