Document Detail


The release of spinal prostaglandin E2 and the effect of nitric oxide synthetase inhibition during strychnine-induced allodynia.
MedLine Citation:
PMID:  11524348     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The removal of spinal glycinergic inhibition by intrathecal strychnine produces an allodynia-like state in rodents. Our objective was to measure spinal prostaglandin E2 (PGE2) release during strychnine-allodynia and examine the effects of Nomega-nitro-L-arginine (L-NOARG), an inhibitor of nitric oxide synthetase. Under halothane, rats were fitted with intrathecal and spinal microdialysis catheters, and microelectrodes implanted into the locus coeruleus for measurement of catechol oxidation current (CAOC) using voltammetry. Animals were then administered urethane and treated as follows: 1) baseline control 10 min, intrathecal strychnine (40 microg) 10 min, 10 min of hair deflection, and 2) 10-min control followed by intrathecal strychnine (40 microg) with hair deflection for 60 min. Spinal dialysate samples were collected for PGE2 levels determined by using immunoassay. In separate experiments, the effect of intrathecal strychnine (40 microg) followed by hair deflection was studied in rats pretreated with intrathecal l-NOARG (50 nmol). After intrathecal strychnine, hair deflection significantly increased spinal PGE2 release (619% +/- 143%), locus coeruleus CAOC (181% +/- 6%), and mean arterial pressure (123% +/- 2%) P < 0.05. Pretreatment with intrathecal l-NOARG significantly inhibited strychnine-allodynia. In this model, hair deflection evokes spinal PGE2 release, locus coeruleus activation, and an increase in mean arterial pressure. L-NOARG pretreatment attenuated the locus coeruleus CAOC, a biochemical index of strychnine-allodynia, suggesting a mediator role of nitric oxide. A mediator role of nitric oxide is also implicated, helping to explain the pathophysiology of this allodynic pain.
Authors:
B Milne; S R Hall; M E Sullivan; C Loomis
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Anesthesia and analgesia     Volume:  93     ISSN:  0003-2999     ISO Abbreviation:  Anesth. Analg.     Publication Date:  2001 Sep 
Date Detail:
Created Date:  2001-08-28     Completed Date:  2001-09-20     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  1310650     Medline TA:  Anesth Analg     Country:  United States    
Other Details:
Languages:  eng     Pagination:  728-33     Citation Subset:  AIM; IM    
Affiliation:
Department of Anesthesiology, Pharmacology, and Toxicology, Queen's University, Kingston, Ontario, Canada.
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MeSH Terms
Descriptor/Qualifier:
Animals
Catechols / metabolism
Dinoprostone / metabolism*
Enzyme Inhibitors / pharmacology*
Hemodynamics / drug effects
Hyperalgesia / chemically induced*,  metabolism*
Male
Nitric Oxide Synthase / antagonists & inhibitors*
Nitric Oxide Synthase Type I
Nitroarginine / pharmacology
Oxidation-Reduction
Physical Stimulation
Poisons*
Rats
Rats, Sprague-Dawley
Spinal Cord / drug effects*,  metabolism*
Strychnine*
Chemical
Reg. No./Substance:
0/Catechols; 0/Enzyme Inhibitors; 0/Poisons; 2149-70-4/Nitroarginine; 363-24-6/Dinoprostone; 57-24-9/Strychnine; EC 1.14.13.39/Nitric Oxide Synthase; EC 1.14.13.39/Nitric Oxide Synthase Type I; EC 1.14.13.39/Nos1 protein, rat

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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