British Journal of Anaesthesia, 2001, Vol. 86, No. 5 618-626
© 2001 The Board of Management and Trustees of the British Journal of Anaesthesia
Correlating in vivo anaesthetic effects with ex vivo receptor density data supports a GABAergic mechanism of action for propofol, but not for isoflurane
1Department of Anesthesiology and 2Department of Pediatrics, University of California-Irvine Medical Center, Orange, California*Corresponding author: Department of Anesthesiology, University of California, Irvine Medical Center, Route 81A, Bldg 53, 101 City Drive South, Orange, CA 92868, USA
Presented in part at the annual meeting of the Association of University Anesthesiologists, May 18–20, 1995, San Diego, California and the annual meeting of the American Society of Anesthesiologists, October 21–25, 1995, Atlanta, GA, USA.
This article is accompanied by Editorial I.
If the in vivo effects of anaesthesia are mediated through a specific receptor system, then a relationship could exist between the regional changes in brain metabolism caused by a particular agent and the underlying regional distribution of the specific receptors affected by that agent. Positron emission tomography data from volunteers studied while unconscious during propofol (n=8) or isoflurane (n=5) anaesthesia were used retrospectively to explore for evidence of relationships between regional anaesthetic effects on brain glucose metabolism and known (ex vivo) regional distribution patterns of human receptor binding sites. The regional metabolic reductions caused by propofol differed significantly from those of isoflurane. Propofol’s reductions negatively correlated most significantly with the regional distribution of [3H]diazepam and [3H]flunitrazepam (benzodiazepine) binding site densities (r=–0.86, P<0.0005; r=–0.79, P<0.005, respectively) and less strongly with [3H]naloxone (opioid) binding density (r=–0.69, P<0.05). Isoflurane’s reductions positively correlated only with muscarinic (acetylcholine) binding density (r=0.85, P<0.05). These findings are consistent with the hypothesis that some of propofol’s in vivo anaesthetic effects may be mediated through a GABAergic mechanism and suggest some of isoflurane’s in vivo effects might involve antagonism of central acetylcholine functioning.
Br J Anaesth 2001; 86: 618–26
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