CJA
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Article
Right arrow Full Text (PDF)
Right arrow Submit a scholarly reply
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
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
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Fukuhara, N.
Right arrow Articles by Nakanishi, O.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Fukuhara, N.
Right arrow Articles by Nakanishi, O.

Canadian Journal of Anesthesia, Vol 45, 1123-1129, Copyright © 1998 by Canadian Anesthesiologists' Society

ARTICLES

Central noradrenergic mediation of nitrous oxide-induced analgesia in rats

N Fukuhara, T Ishikawa, H Kinoshita, L Xiong and O Nakanishi
Department of Anaesthesiology-Resuscitology, Yamaguchi University School of Medicine, Japan.

PURPOSE: Although several studies have demonstrated that both supra opiate receptors and spinal alpha 2 adrenoceptors play a mediating role in nitrous oxide(N2O) analgesia, controversy still exists. The present study was undertaken to evaluate further the involvement of noradrenergic (NA) neuronal activity in N2O analgesia by investigating tail-flick latency and supra- and spinal NA levels in rats. METHODS: In an analgesia study, effect of N2O 75% and its modification were evaluated using the tail-flick test in male Wistar rats. Results were expressed as % maximum possible effect (MPE). Modification of N2O analgesia was examined in rats pretreated with either the alpha 2 receptor agonist, clonidine(CLO: 150 micrograms.kg-1, i.p.), alpha 2 receptor antagonist, idazoxone(IDZ: 100 micrograms.kg-1, i.v.) by lesioning the locus coeruleus (LC) seven days before exposure to N2O, or naloxone (5 mg.kg-1, i.v.). Also, in a NAergic neuronal transmission study, the changes in NA content at LC and spinal cord were determined using HPLC-ECD. RESULTS: Nitrous oxide produced analgesia, % MPE increased to a maximum of 78% at 30 min, thereafter declining to 38% at 120 min. Clonidine potentiated the analgesic effect of N2O at 120 min (80%). The analgesic effect of N2O was attenuated by IDZ or by LC lesioning. However, naloxone, in a dose sufficient to block morphine-induced analgesia, had no effect. With N2O exposure, NA content was decreased by 52% in the LC and by 20% at spinal cord. With morphine, NA content did not differ from the control group. CONCLUSION: The data suggest that N2O-induced analgesia is principally mediated by activation of the descending inhibitory NAergic system and/or increased NA release at spinal cord which may lead to presynaptic inhibition of primary afferent neurotransmitter release and hyperpolarize the dorsal horn neurons by alpha 2 receptors.


This article has been cited by other articles:


Home page
 Anesth. Analg.Home page
S. K. Georgiev, A. Wakai, T. Kohno, T. Yamakura, and H. Baba
Actions of Norepinephrine and Isoflurane on Inhibitory Synaptic Transmission in Adult Rat Spinal Cord Substantia Gelatinosa Neurons
Anesth. Analg., January 1, 2006; 102(1): 124 - 128.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1998 by the Canadian Anesthesiologists' Society.