• Shannon L Bianchi, Breanna M Caltagarone, Frank M Laferla, Roderic G Eckenhoff, and Max B Kelz.
• Department of Anesthesiology and Critical Care, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA.
• Anesth. Analg. 2010 Feb 1; 110 (2): 427-30.

BackgroundThe number of elderly patients with frank or incipient Alzheimer's disease (AD) requiring surgery is growing as the population ages. General anesthesia may exacerbate symptoms of and the pathology underlying AD, so minimizing anesthetic exposure may be important. This requires knowledge of whether the continuing AD pathogenesis alters anesthetic potency.MethodsWe determined the induction potency and emergence time for isoflurane, halothane, and sevoflurane using the minimum alveolar anesthetic concentration for loss of righting reflex as an end point in 12- to 14-mo-old triple transgenic Alzheimer (3xTgAD) mice and wild type C57BL6 controls. 3xTgAD mice model AD by harboring three distinct mutations: the APP(Swe), Tau, and PS1 human transgenes, each of which has been associated with familial forms of human AD.ResultsThe 3xTgAD mice exhibited mild resistance (from 8% to 30%) to volatile anesthetics but displayed indistinguishable emergence patterns from all three inhaled anesthetics.ConclusionsThese results show that the genetic vulnerabilities and neuropathology associated with AD produce a small but significant decrease in sensitivity to the hypnotic actions of three inhaled anesthetics. Emergence times were not altered.

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