JOURNAL HOME CME HOME THIS MONTH PAST ISSUES ETOC COLLECTIONS
AUTHORS REVIEWERS EDITORIAL BOARD FEEDBACK RSS HELP
A&A International Anesthesia Research Society
QUICK SEARCH:   [advanced]


     

Anesth Analg 2008; 107:875-878
© 2008 International Anesthesia Research Society
doi: 10.1213/ane.0b013e3181815fbc
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a colleague
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Google Scholar
Right arrow Articles by Zhang, Y.
Right arrow Articles by Harris, R. A.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Zhang, Y.
Right arrow Articles by Harris, R. A.
Related Collections
Right arrow Mechanisms
Right arrow Preclinical Pharmacology
Right arrow Pharmacology

ANESTHETIC PHARMACOLOGY

Intrathecal Veratridine Administration Increases Minimum Alveolar Concentration in Rats

Yi Zhang, MD*, Manohar Sharma, PhD{dagger}, Edmond I. Eger, II, MD{dagger}, Michael J. Laster, DVM{dagger}, Hugh C. Hemmings, Jr, MD, PhD{ddagger}, and R. Adron Harris, PhD§

From the *Department of Anesthesiology, Fuwai Hospital and Cardiovascular Institute, Beijing, China; {dagger}Department of Anesthesia and Perioperative Care, University of California, San Francisco, California; {ddagger}Department of Anesthesiology and Pharmacology, Weill Cornell Medical College of Cornell University, New York, New York; and §Waggoner Center for Alcohol and Addiction Research, The University of Texas, Austin, Texas.

Address correspondence and reprint requests to Dr. Eger, Department of Anesthesia, S-455, University of California, San Francisco, CA 94143-0464. Address e-mail to egere{at}anesthesia.ucsf.edu.

BACKGROUND: Results from several studies point to sodium channels as potential mediators of the immobility produced by inhaled anesthetics. We hypothesized that the intrathecal administration of veratridine, a drug that enhances the activity or effect of sodium channels, should increase MAC.

METHODS: We measured the change in isoflurane MAC caused by intrathecal infusion of various concentrations of veratridine into the lumbothoracic subarachnoid space of rats. We compared these result with those obtained from intracerebroventricular infusion.

RESULTS: As predicted, intrathecal infusion of veratridine increased MAC. The greatest infused concentration (25 µM) also produced neuronal injury in the hindlimbs of two rats and decreased the peak effect on MAC. A concentration of 1.6 µM produced the largest (21%) increase in MAC. Intraventricular infusion of 1.6 and 6.4 µM veratridine did not alter MAC. Rats given 25 µM died.

CONCLUSIONS: Intrathecal administration of veratradine increases MAC of isoflurane, a finding consistent with a role for sodium channels as potential mediators of the immobility produced by inhaled anesthetics.




This article has been cited by other articles:


Home page
 Anesth. Analg.Home page
E. I. Eger II, D. E. Raines, S. L. Shafer, H. C. Hemmings Jr, and J. M. Sonner
Is a New Paradigm Needed to Explain How Inhaled Anesthetics Produce Immobility?
Anesth. Analg., September 1, 2008; 107(3): 832 - 848.
[Abstract] [Full Text] [PDF]


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 © 2008 by the International Anesthesia Research Society.