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 1987; 66:1090-1095
© 1987 International Anesthesia Research Society
This Article
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
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Todd, M. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Todd, M. M.

The Effects of Paco2 on the Cerebrovascular Response to Nitrous Oxide in the Halothane-Anesthetized Rabbit

Michael M. Todd, MD

Received from the Neuroanesthesia Research Group, Department of Anesthesiology, University of Iowa Hospitals and Clinics, Iowa City, Iowa.

Abstract

Several authors have observed that nitrous oxide increases cerebral blood flow (CBF) and/or intracranial pressure (ICP) in experimental situations and in humans. However, the effects of hippomania on the cerebrovascular responses to NzO have not been investigated. Therefore, six New Zealand White rabbits were anesthetized with ssmile1.0 MAC halothane (mean end-tidal concentration 1.26%) and surgically prepared for recording of ICP, the EEG, and both cortical and global CBF (by the H2-clearance method). After preparation was complete, measurements were obtained during ventilation with 70% nitrogen (in O2), and after the inspired gas mixture was changed to 70% N2O (still with 1.0 MAC halothane). Two such data pairs (N2-N2O) were obtained, one during hypocarbia (Paco2 ssmile 20 mm Hg) and the other during normocarbic (Paco2 ssmile 40 mm Hg) conditions. Mean arterial pressure (MABP) was held constant within each data pair by infusing angiotensin II as needed.

Nitrous oxide resulted in a consistent increase in EEG frequency and decrease in amplitude as compared with N2, and produced small (ssmile1 mm Hg) but statistically significant increases in ICP during both hypo-and normocarbic conditions. Nitrous oxide administration also increased CBF as measured both in frontal cortex and globally, with similar changes seen during hypo-and normocarbic conditions, e.g., cortical CBF increased from 42 ± 8 to 59 ± 15 ml·100 gm–1·min–1 during hypocarbia, and from 61 ± 13 to 75 ± 15 ml·100gm–1·min–1 during normocarbia. These results confirm that N2O is a potent cerebrovasodilator in the rabbit, and also indicate that reductions in Paco2 do not blunt the cerebrovascular responses to N2O.

Key Words: ANESTHESIA—neurosurgical • ANESTHETICS, VOLATILE—halothane • ANESTHETICS, GASEOUS—nitrous oxide • BRAIN—blood flow, electroencephalography, intracranial pressure




This article has been cited by other articles:


Home page
Anesth. Analg.Home page
M. Aono, J. Sato, and T. Nishino
Nitrous Oxide Increases Normocapnic Cerebral Blood Flow Velocity but Does Not Affect the Dynamic Cerebrovascular Response to Step Changes in End-Tidal PCO2 in Humans
Anesth. Analg., September 1, 1999; 89(3): 684 - 684.
[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 © 1987 by the International Anesthesia Research Society.