Skip Navigation



BJA Advance Access published online on January 23, 2006
British Journal of Anaesthesia, doi:10.1093/bja/ael010
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
96/3/361    most recent
ael010v1
Right arrow E-Letters: Submit a response to the article
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
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 Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Engelhardt, T.
Right arrow Articles by Webster, N. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Engelhardt, T.
Right arrow Articles by Webster, N. R.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Board of Management and Trustees of the British Journal of Anaesthesia 2006. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org
Accepted December 1, 2005

Laboratory Investigation

Inhibition of neuronal nitric oxide synthase reduces isoflurane MAC and motor activity even in nNOS knockout mice

T. Engelhardt 1 *, P. R. Lowe 1, H. F. Galley 1, and N. R. Webster 1

1 Academic Unit of Anaesthesia and Intensive Care, Institute of Medical Sciences, University of Aberdeen, Aberdeen AB25 2ZD, Scotland, UK

* To whom correspondence should be addressed.
T. Engelhardt, E-mail: t.engelhardt{at}abdn.ac.uk


  Abstract

Background. The glutamate-nitric oxide-cyclic GMP pathway has been identified as a potential target for volatile anaesthetic agents as acute inhibition of nitric oxide synthase (NOS) reduces the minimum alveolar concentration (MAC) in most animal studies. However, mice deficient in the type I NOS isoform (nNOS) are reported to have a similar MAC for isoflurane and are not affected by non-isoform specific inhibitors.

Methods. We determined whether the nNOS specific inhibitor, 7-nitroindazole (7-NI), had an effect on isoflurane MAC and righting reflex (RRF) and investigated spontaneous motor activity in an open-field study in wild-type (WT) and knockout (KO) mice.

Results. 7-NI reduced isoflurane MAC and RRF in both WT and KO animals (all P<0.04). 7-NI profoundly reduced spontaneous motor activity in both the WT and KO animals in the open-field study as indicated by a reduction in the number of line crossings and rearings in both WT and KO mice (both P<0.001).

Conclusion. We conclude that isoform specific inhibition of nNOS reduces MAC and spontaneous motor activity even in nNOS KO animals. Our results indicate that the NMDA receptor-nitric oxide-cyclic GMP pathway remains a credible target in modulating the effects of isoflurane.

Keywords: anaesthetics volatile, isoflurane; inhibitor, 7-NI; isoform, nNOS; mice, open-field.
Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


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]

Home page
 Br J AnaesthHome page
M. Smith and R. P. Mahajan
Clinical neuroscience: relevance to current practice
Br. J. Anaesth., July 1, 2007; 99(1): 1 - 3.
[Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.