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Inhaled Anesthetic Potency in Aged Alzheimer Mice

Shannon L. Bianchi, MD^*, Breanna M. Caltagarone, MS^*, Frank M. LaFerla, PhD, Roderic G. Eckenhoff, MD^*,, and Max B. Kelz, MD, PhD^*,,,||

From the *Department of Anesthesiology and Critical Care, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania; Department of Neurobiology and Behavior, Institute for Brain Aging and Dementia, University of California, Irvine, Irvine, California; and Institute for Translational Medicine and Therapeutics, Mahoney Institute for Neurological Science, and ||Center for Sleep and Respiratory Neurobiology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania.

Address correspondence and reprint requests to Max B. Kelz, MD, PhD, Department of Anesthesiology and Critical Care, University of Pennsylvania School of Medicine, 3620 Hamilton Walk, 334 John Morgan Building, Philadelphia, PA 19104. Address e-mail to kelzma{at}uphs.upenn.edu.

Abstract

Background: The 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.

Methods: We 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.

Results: The 3xTgAD mice exhibited mild resistance (from 8% to 30%) to volatile anesthetics but displayed indistinguishable emergence patterns from all three inhaled anesthetics.

Conclusions: These 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.