The release of spinal prostaglandin E2 and the effect of nitric oxide synthetase inhibition during strychnine-induced allodynia

Citation
B. Milne et al., The release of spinal prostaglandin E2 and the effect of nitric oxide synthetase inhibition during strychnine-induced allodynia, ANESTH ANAL, 93(3), 2001, pp. 728-733
Citations number
26
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Aneshtesia & Intensive Care","Medical Research Diagnosis & Treatment
Journal title
ANESTHESIA AND ANALGESIA
ISSN journal
0003-2999 → ACNP
Volume
93
Issue
3
Year of publication
2001
Pages
728 - 733
Database
ISI
SICI code
0003-2999(200109)93:3<728:TROSPE>2.0.ZU;2-4
Abstract
The removal of spinal glycinergic inhibition by intrathecal strychnine prod uces an allodynia-like state in rodents, Our objective was to measure spina l prostaglandin E2 (PGE2) release during strychnine-allodynia and examine t he effects of N omega -nitro-L-arginine (L-NOARG), an inhibitor of nitric o xide synthetase. Under halothane, rats were fitted with intrathecal and spi nal microdialysis catheters, and microelectrodes implanted into the locus c oeruleus for measurement of catechol oxidation current (CAOC) using voltamm etry. Animals were then administered urethane and treated as follows: 1) ba seline control 10 min, intrathecal strychnine (40 mug) 10 min, 10 min of ha ir deflection, and 2) 10-min control followed by intrathecal strychnine (40 mug) with hair deflection for 60 min. Spinal dialysate samples were collec ted for PGE2 levels determined by using immunoassay. In separate experiment s, the effect of intrathecal strychnine (40 mug) followed by hair deflectio n 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 arte rial pressure (123% +/- 2%) P < 0.05. Pretreatment with intrathecal L-NOARG significantly inhibited strychnine-allodynia. In this model, hair deflecti on evokes spinal PGE2 release, locus coeruleus activation, and an increase in mean arterial pressure. L-NOARG pretreatment attenuated the locus coerul eus CAOC, a biochemical index of strychnine-allodynia, suggesting a mediato r role of nitric oxide. A mediator role of nitric oxide is also implicated, helping to explain the pathophysiology of this allodynic pain.