Linked Life Data

1727747

Source:http://linkedlifedata.com/resource/pubmed/id/1727747

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1992-1-30
pubmed:abstractText
The effects of colonic inflammation induced by trinitrobenzene sulfonic acid and influence of previous treatment with specific antagonists of inflammatory mediators (platelet-activating factor, leukotrienes, prostaglandins, and thromboxanes) on colonic transit were examined in conscious rats which were permanently fitted with an intracolonic catheter inserted into the proximal colon. Colonic inflammation was induced by intracolonic administration of trinitrobenzene acid (80 mg/kg) in 50% ethanol. Colonic transit time was evaluated by intracolonic administration of a radiolabeled marker [( 51Cr]sodium chromate) and collection of the feces per hour on a conveyor belt. Excretion of the marker was then plotted vs. time, permitting calculations of the times elapsed to recover 25%, 50%, and 75% of the marker injected (T25, T50, and T75, respectively). In control (saline) animals, excretion of the marker described a regular sigmoid curve with 50% of the marker recovered at 6.92 +/- 0.40 hours after intracolonic administration (T25 = 6.4 +/- 0.43 hours; T75 = 7.49 +/- 0.39 hours). Ethanol (vehicle), 50%, did not modify the profile of marker recovery. On the contrary, single intracolonic administration of trinitrobenzene sulfonic acid/ethanol induced a biphasic response consisting of an early pool of radiolabeled feces (T25 = 4.03 +/- 0.55 hours) with a delayed total one (T50 = 11.74 +/- 0.83 hours; T75 = 13.70 +/- 0.49 hours). Antagonists of the leukotriene pathway, i.e., MK = 886, a lipoxygenase inhibitor, and SKF 104,353 and SR 2640, two different leukotriene D4 receptor antagonists, blocked the effects of trinitrobenzene sulfonic acid on colonic transit time and restored a control profile of radiolabeled marker excretion. In contrast, indomethacin, a cyclooxygenase inhibitor, and SC 19220, a specific prostaglandin E2 receptor antagonist, were inefficient in blocking the effects of trinitrobenzene sulfonic acid on colonic transit time. Specific thromboxane A2 receptor antagonists, KT1-32 and GR 32191B, did not show any improvement in colonic transit after trinitrobenzene sulfonic acid administration. Previous injection of the specific platelet-activating factor receptor antagonists, BN 52021 or BN 50730, was also unable to restore a normal marker excretion profile after administration of trinitrobenzene sulfonic acid. It is concluded that the alterations of colonic transit immediately observed after intracolonic trinitrobenzene sulfonic acid administration are mediated through the release of leukotriene D4. In contrast, platelet-activating factor, prostaglandins, and thromboxanes are not involved in the mediation of these transit disturbances.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0016-5085
pubmed:author
pubmed:issnType
Print
pubmed:volume
102
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
149-56
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1992
pubmed:articleTitle
Leukotriene D4 participates in colonic transit disturbances induced by intracolonic administration of trinitrobenzene sulfonic acid in rats.
pubmed:affiliation
Department of Pharmacology-Toxicology, Institut National de la Recherche Agronomique, Toulouse, France.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't