JOURNAL HOME CME HOME THIS MONTH PAST ISSUES ETOC COLLECTIONS AUTHORS REVIEWERS EDITORIAL BOARD FEEDBACK RSS HELP
		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a colleague Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Rorie, D. K. Articles by Sill, J. C. Search for Related Content PubMed PubMed Citation Articles by Rorie, D. K. Articles by Sill, J. C.

Increased Norepinephrine Release from Dog Pulmonary Artery Caused by Nitrous Oxide

Received from the Departments of Anesthesiology, Physiology and Biophysics, Mayo Clinic and Mayo Foundation, Rochester, Minnesota.

Abstract

The effects of nitrous oxide on the release and metabolism of norepinephrine (NE) at neuroeffector junctions in dog pulmonary artery were examined. Helical strips of artery were incubated in Krebs-Ringer solution containing L-(³H)NE and mounted for superfusion. The arterial strips were studied in the presence of 1) 95% oxygen-5% carbon dioxide, 2) 70% nitrogen-30% oxygen, or 3) 70% nitrous ox- ide-30% oxygen. During the 60 min of each experiment, five samples of superfusion fluid were collected for analysis and the effluxes of (³H)NE and its radiolabeled metabolities were measured before and during electrical stimulation and during recovery from stimulation. (³H)Norepinephrine was separated from its metabolites in the superfusate and in extracts of artery by column chromatography and quantitated by liquid scintillation spectrometry. Nitrous oxide significantly increased the fractional loss of total radioactivity and the amount of NE in the superfusate both during resting conditions and during stimulation. Nitrous oxide had no effect on the proportions of radioactivity among metabolites of NE in the superfusate or on the profile of NE metabolites remaining in the tissue after experimentation. These findings are consistent with increased NE release as a direct effect of nitrous oxide on nerve endings.

Key Words: ANESTHETICS, GASES—nitrous oxide • SYMPATHETIC NERVOUS SYSTEM—nitrous oxide

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