Document Detail

Excess nitric oxide does not cause cellular, vascular, or mucosal dysfunction in the cat small intestine.
MedLine Citation:
PMID:  7631799     Owner:  NLM     Status:  MEDLINE    
The overproduction of nitric oxide in the small bowel has been invoked as a cytotoxic event in the vascular, mucosal, and whole organ dysfunction associated with inflammation. We assessed whether exogenous administration of nitric oxide in the form of nitric oxide donors (CAS 754, SIN-1) could cause microvascular and mucosal barrier dysfunction in vivo or epithelial and endothelial cell permeability alterations and cell injury in vitro. Increasing concentrations of CAS 754 or SIN-1 were infused locally into autoperfused segments of cat ileum at 30-min intervals. Baseline epithelial permeability (blood-to-lumen clearance of 51Cr-EDTA) was not affected by CAS 754, whereas vascular protein clearance was reduced. The latter effect could almost entirely be explained by a decrease in intestinal capillary hydrostatic pressure. Therefore, in some experiments venous pressure was elevated and the microvascular reflection coefficient for total proteins was estimated at filtration-independent rates. This direct measurement of microvascular permeability was unaffected by exogenous nitric oxide. CAS 754 did not increase permeability across monolayers of endothelial or epithelial cells and did not cause cell injury. Next, we assessed the possibility that excess nitric oxide may be detrimental, but only in inflamed intestine, by infusing CAS 754 with platelet-activating factor; the latter directly increases microvascular and mucosal permeability. CAS 754 did not exacerbate but rather reduced platelet-activating factor-induced rise in microvascular and mucosal permeability. These results suggest that high concentrations of nitric oxide do not cause breakdown of mucosal or microvascular barrier integrity under normal or inflammatory conditions.
P Kubes; P H Reinhardt; D Payne; R C Woodman
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The American journal of physiology     Volume:  269     ISSN:  0002-9513     ISO Abbreviation:  Am. J. Physiol.     Publication Date:  1995 Jul 
Date Detail:
Created Date:  1995-09-01     Completed Date:  1995-09-01     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0370511     Medline TA:  Am J Physiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  G34-41     Citation Subset:  IM    
Department of Medical Physiology, University of Calgary Medical Center, Alberta, Canada.
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MeSH Terms
Blood Vessels / physiology
Capillary Permeability / drug effects
Dose-Response Relationship, Drug
Edetic Acid / pharmacokinetics
Intestinal Mucosa / physiology*
Intestine, Small / drug effects,  physiology*
Intestines / blood supply*
Molsidomine / analogs & derivatives,  pharmacology
Nitric Oxide / metabolism*
Permeability / drug effects
Platelet Activating Factor / pharmacology
Sydnones / pharmacology
Reg. No./Substance:
0/Platelet Activating Factor; 0/Sydnones; 10102-43-9/Nitric Oxide; 137500-42-6/3-(cis-2,6-dimethylpiperidino)sydnonimine; 25717-80-0/Molsidomine; 33876-97-0/3-morpholino-sydnonimine; 60-00-4/Edetic Acid

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

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