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Anesth Analg 2005;101:1362-1367
© 2005 International Anesthesia Research Society
doi: 10.1213/01.ANE.0000180832.62367.CC

ANESTHETIC PHARMACOLOGY

Nitric Oxide Is Not a Mediator of Inflammation-Induced Resistance to Atracurium

Heidrun Fink, MD*§, Ralph Bogdanski, MD*, Peter Luppa, MD#, J. A. Jeevendra Martyn, MD§, and Manfred Blobner, MD*

*Klinik für Anaesthesiologie der Technischen Universität München and #Institut für Klinische Chemie und Pathobiochemie der Technischen Universität München, Klinikum rechts der Isar, Munich, Germany; and §Department of Anesthesiology and Critical Care, Harvard Medical School and Anesthesia Services, Massachusetts General Hospital, and Shriners Hospital for Children, Boston, MA

Address correspondence to Heidrun Fink, MD, Klinik für Anaesthesiologie der Technischen Universität München*, Klinikum rechts der Isar, Ismaninger Str. 22, 81675 Munich, Germany. Address electronic mail to h.fink{at}lrz.tum.de.

Resistance to atracurium as a result of increased drug binding to {alpha}1-acid glycoprotein is associated with increased inducible nitric oxide synthase activity and increased nitric oxide levels in plasma. We investigated if the inhibition of inducible nitric oxide synthase and suppression of nitric oxide can reverse the resistance to atracurium. As a model of {alpha}1-acid glycoprotein and nitric oxide increase, 84 male Sprague-Dawley rats received an IV injection of either 60 mg/kg Corynebacterium parvum (CP) or saline (control). The 2 groups (CP/Control) were further divided into subgroups, receiving the selective inducible nitric oxide synthase inhibitor, N-Iminolysine, via drinking water at different concentrations. On day 4 post-CP injection, the pharmacodynamics of atracurium were determined. Plasma concentrations of nitric oxide, atracurium, and {alpha}1-acid glycoprotein were measured and acetylcholine receptor numbers were quantified. In the CP groups, N-Iminolysine suppressed nitric oxide levels in a dose-dependent manner. Resistance to atracurium persisted. {alpha}1-acid glycoprotein serum levels remained increased in all CP groups with no differences in acetylcholine receptor expression. Our results suggest that the mechanism leading to increased expression of {alpha}1-acid glycoprotein and consecutive increased protein binding of atracurium is not mediated by inducible nitric oxide synthase induction and nitric oxide expression.






Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press
Copyright © 2005 by the International Anesthesia Research Society.