Mechanisms of actions of anaesthetic drugs

Current Opinion in Anaesthesiology

Volumn 10, Issue 4, 1997, Pages 261-266

  Bovill, James G ^a  

^a LEIDEN UNIVERSITY MEDICAL CENTER   (Netherlands)

Author keywords

[No Author keywords available]

Indexed keywords

4 AMINOBUTYRIC ACID A RECEPTOR; ALFAXALONE; ANESTHETIC AGENT; BARBITURIC ACID DERIVATIVE; CALCIUM CHANNEL; ENFLURANE; ETOMIDATE; GLYCINE RECEPTOR; HALOTHANE; ISOFLURANE; KETAMINE; N METHYL DEXTRO ASPARTIC ACID RECEPTOR; NICOTINIC RECEPTOR; PHOSPHOLIPASE A2; POTASSIUM CHANNEL; PROPOFOL; PROTEIN KINASE C; SODIUM CHANNEL; VOLTAGE GATED CHANNEL FORMING PROTEIN;

ANESTHESIA; DRUG MECHANISM; INHALATIONAL DRUG ADMINISTRATION; INTRAVENOUS DRUG ADMINISTRATION; NAUSEA; PRIORITY JOURNAL; REVIEW; VOMITING;

EID: 0030849105     PISSN: 09527907     EISSN: None     Source Type: Journal    
DOI: 10.1097/00001503-199708000-00005     Document Type: Review

References (39)

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10. + channels, although their mechanisms of action appear to be different. The inhibition of potassium currents would increase neuronal excitability, possibly activating inhibitory pathways within the brain, thereby contributing to anaesthesia. It is also possible that increased neuronal excitability may contribute to the excitatory phase during induction of anaesthesia.
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38. 2 in the action of general anaesthetics. Am J Physiol 1996, 270:C636-C644. The results of this study suggest that anaesthetics produce their effect on BK potassium channels by disrupting the phospholipase-arachidonic acid signal transduction pathway. This provides an interesting link between the conflicting descriptions of anaesthetic action, namely the lipid phase theory based on the Meyer-Overton rule and the theory that suggests that anaesthetic actions are the result of interactions with specific receptor sites.
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