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]


     

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 ISI Web of Science
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 ISI Web of Science (8)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Hoffman, W. E.
Right arrow Articles by Koenig, H. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hoffman, W. E.
Right arrow Articles by Koenig, H. M.
Anesth Analg 2001;93:166-170
© 2001 International Anesthesia Research Society

NEUROSURGICAL ANESTHESIA

Sodium Nitroprusside Compared with Isoflurane-Induced Hypotension: The Effects on Brain Oxygenation and Arteriovenous Shunting

William E. Hoffman, PhD, Guy Edelman, MD, Rick Ripper, CVT, and Heidi M. Koenig, MD

Department of Anesthesiology, University of Illinois at Chicago, Chicago, Illinois

Address correspondence and reprint requests to William E. Hoffman, PhD, Department of Anesthesiology, M/C 515, University of Illinois at Chicago, 1740 W. Taylor St., Chicago, IL 60612. Address e-mail to whoffman{at}uic.edu

We compared sodium nitroprusside (SNP)-induced hypotension with 3% isoflurane-induced hypotension with regard to brain tissue oxygen pressure (PtO2), middle cerebral artery (MCA) blood flow, and cerebral arteriovenous shunting. Eight dogs were anesthetized with 1.5% isoflurane. After a craniotomy, a probe was inserted into the left frontoparietal brain cortex to mea-sure tissue gases and pH. Blood flow was measured in a secondary branch of the MCA by a flowprobe. Mea-surements were made during baseline 1.5% isoflurane, during 1.5% isoflurane and SNP-induced hypotension or 3% isoflurane-induced hypotension to a mean pressure of 60–65 mm Hg, and during continued treatment with SNP or 3% isoflurane with blood pressure support to baseline levels with phenylephrine. Shunting was calculated from arterial, sagittal sinus, and tissue (indicating capillary) oxygen content. During hypotension with SNP, PtO2 decreased 50%, and shunting increased 50%. During hypotension with 3% isoflurane, PtO2 and shunting did not change. Blood pressure support increased PtO2 and MCA flow during both SNP and 3% isoflurane treatment. These results show that SNP is a cerebrovasodilator but that hypotension will decrease PtO2, probably because of an increase in arteriovenous shunting and a decrease in capillary perfusion.

Implications: We measured brain arteriovenous shunting and tissue oxygen pressure(PtO2)during a 40% decrease in blood pressure induced by sodium nitroprusside (SNP)or 3% isoflurane. Large-dose isoflurane maintainedPtO2 withno change in shunting. SNP infusion decreasedPtO2 50%and increased shunting 50%. This suggests that SNP-induced hypotensiondecreasesPtO2because of a decrease in capillaryperfusion.






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 © 2001 by the International Anesthesia Research Society.