A1 Journal article – refereed
Comparative effects of dexmedetomidine, propofol, sevoflurane, and S-ketamine on regional cerebral glucose metabolism in humans: a positron emission tomography study

List of Authors: Laaksonen L., Kallioinen M., Långsjö J., Laitio T., Scheinin A., Scheinin J., Kaisti K., Maksimow A., Kallionpää R.E., Rajala V., Johansson J., Kantonen O., Nyman M., Sirén S., Valli K., Revonsuo A., Solin O., Vahlberg T., Alkire M., Scheinin H.
Publication year: 2018
Journal: British Journal of Anaesthesia
Journal acronym: BRIT J ANAESTH
Volume number: 121
Issue number: 1
Number of pages: 10
ISSN: 0007-0912
eISSN: 1471-6771


Introduction: The highly selective alpha(2)-agonist dexmedetomidine has become a popular sedative for neurointensive care patients. However, earlier studies have raised concern that dexmedetomidine might reduce cerebral blood flow without a concomitant decrease in metabolism. Here, we compared the effects of dexmedetomidine on the regional cerebral metabolic rate of glucose (CMRglu) with three commonly used anaesthetic drugs at equi-sedative doses.

Methods: One hundred and sixty healthy male subjects were randomised to EC50 for verbal command of dexmedetomidine (1.5 ng ml (1); n=40), propofol (1.7 mu g ml (1); n=40), sevoflurane (0.9% end-tidal; n=40) or S-ketamine (0.75 mu g ml (1); n=20) or placebo (n=20). Anaesthetics were administered using target-controlled infusion or vapouriser with end-tidal monitoring. F-18-labelled fluorodeoxyglucose was administered 20 min after commencement of anaesthetic administration, and high-resolution positron emission tomography with arterial blood activity samples was used to quantify absolute CMRglu for whole brain and 15 brain regions.

Results: At the time of [F-18]fluorodeoxyglucose injection, 55% of dexmedetomidine, 45% of propofol, 85% of sevoflurane, 45% of S-ketamine, and 0% of placebo subjects were unresponsive. Whole brain CMRglu was 63%, 71%, 71%, and 96% of placebo in the dexmedetomidine, propofol, sevoflurane, and S-ketamine groups, respectively (P<0.001 between the groups). The lowest CMRglu was observed in nearly all brain regions with dexmedetomidine (P<0.05 compared with all other groups). With S-ketamine, CMRglu did not differ from placebo.

Conclusions: At equi-sedative doses in humans, potency in reducing CMRglu was dexmedetomidine>propofol>ketamine=placebo. These findings alleviate concerns for dexmedetomidine-induced vasoconstriction and cerebral ischaemia.

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Last updated on 2019-09-07 at 18:00