Abstract | BACKGROUND & AIMS: METHODS:
Zymosan or saline was given intracolonically, and the visceromotor response to noxious colorectal distention (80 mm Hg, 20 seconds) was measured 3 hours afterward. RESULTS: There was a significant enhancement of the visceromotor response in zymosan-, but not saline-treated, rats. This hyperalgesia was dose-dependently and reversibly attenuated by intrathecal administration of the nonselective NO* synthase (NOS) inhibitor NG-nitro-L-arginine methyl ester (100-800 nmol) as well as by the selective neuronal NOS inhibitor ARL 17477 (30-600 nmol). In support of these observations, there was a significant increase in the number of cells labeled for NADPH diaphorase or neuronal NOS in the lumbosacral spinal cord after intracolonic instillation of zymosan, but not saline. CONCLUSIONS: These data suggest that colonic inflammation induces the expression of neuronal NOS in the spinal cord and that increased production of spinal NO* is necessary for maintenance of zymosan-produced visceral hyperalgesia.
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Authors | S V Coutinho, G F Gebhart |
Journal | Gastroenterology
(Gastroenterology)
Vol. 116
Issue 6
Pg. 1399-408
(Jun 1999)
ISSN: 0016-5085 [Print] United States |
PMID | 10348823
(Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.)
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Chemical References |
- Enzyme Inhibitors
- Nitric Oxide
- Zymosan
- Nitric Oxide Synthase
- Nitric Oxide Synthase Type I
- Nos1 protein, rat
- NADPH Dehydrogenase
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Topics |
- Abdominal Muscles
(physiopathology)
- Animals
- Colon
- Enzyme Inhibitors
(pharmacology)
- Hindlimb
- Hyperalgesia
(chemically induced, metabolism, physiopathology)
- Injections
- Injections, Spinal
- Male
- Muscle Contraction
(physiology)
- Muscle, Skeletal
(physiopathology)
- NADPH Dehydrogenase
(metabolism)
- Nitric Oxide
(physiology)
- Nitric Oxide Synthase
(antagonists & inhibitors, metabolism)
- Nitric Oxide Synthase Type I
- Rats
- Rats, Sprague-Dawley
- Spinal Cord
(metabolism)
- Viscera
(physiopathology)
- Zymosan
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