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  • 1. Kunst, Gudrun
    et al.
    Milojevic, Milan
    Boer, Christa
    De Somer, Filip M. J. J.
    Gudbjartsson, Tomas
    van den Goor, Jenny
    Jones, Timothy J.
    Lomivorotov, Vladimir
    Merkle, Frank
    Ranucci, Marco
    Puis, Luc
    Wahba, Alexander
    Alston, Peter
    Fitzgerald, David
    Nikolic, Aleksandar
    Onorati, Francesco
    Rasmussen, Bodil Steen
    Svenmarker, Staffan
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine. Heart Center, Umeå University, Umeå..
    2019 EACTS/EACTA/EBCP guidelines on cardiopulmonary bypass in adult cardiac surgery2019In: British Journal of Anaesthesia, ISSN 0007-0912, E-ISSN 1471-6771, Vol. 123, no 6, p. 713-757Article, review/survey (Refereed)
  • 2. Laaksonen, L.
    et al.
    Kallioinen, M.
    Löngsjö, J.
    Laitio, T.
    Scheinin, A.
    Scheinin, J.
    Kaisti, K.
    Maksimow, A.
    Kallionpää, R. E.
    Rajala, V.
    Johansson, Jarkko
    Umeå University, Faculty of Medicine, Department of Radiation Sciences. Turku PET Centre, University of Turku and Turku University Hospital, Turku, Finland.
    Kantonen, O.
    Nyman, M.
    Sirén, S.
    Valli, K.
    Revonsuo, A.
    Solin, O.
    Vahlberg, T.
    Alkire, M.
    Scheinin, H.
    Comparative effects of dexmedetomidine, propofol, sevoflurane, and S-ketamine on regional cerebral glucose metabolism in humans: a positron emission tomography study2018In: British Journal of Anaesthesia, ISSN 0007-0912, E-ISSN 1471-6771, Vol. 121, no 1, p. 281-290Article in journal (Refereed)
    Abstract [en]

    Introduction: The highly selective α2-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 μg ml-1; n=40), sevoflurane (0.9% end-tidal; n=40) or S-ketamine (0.75 μg ml−1; n=20) or placebo (n=20). Anaesthetics were administered using target-controlled infusion or vapouriser with end-tidal monitoring. 18F-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 [F18]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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