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The role of the enzyme cyclooxygenas...

Campbell, Nigel Brent.

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The role of the enzyme cyclooxygenase and bile in the damage and repair of intestinal epithelium.

Record Type:	Electronic resources : Monograph/item
Title/Author:	The role of the enzyme cyclooxygenase and bile in the damage and repair of intestinal epithelium./
Author:	Campbell, Nigel Brent.
Description:	164 p.
Notes:	Source: Dissertation Abstracts International, Volume: 64-10, Section: B, page: 4704.
Contained By:	Dissertation Abstracts International64-10B.
Subject:	Biology, Animal Physiology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3107752
ISBN:	9780496553006

The role of the enzyme cyclooxygenase and bile in the damage and repair of intestinal epithelium.
Campbell, Nigel Brent.

The role of the enzyme cyclooxygenase and bile in the damage and repair of intestinal epithelium. - 164 p.

Source: Dissertation Abstracts International, Volume: 64-10, Section: B, page: 4704.

Thesis (Ph.D.)--North Carolina State University, 2003.

Colic describes poorly localized abdominal pain and is treated with nonsteroidal anti-inflammatory drugs (NSAIDs). They inhibit the enzyme cyclooxygenase (COX), which has two isoforms: COX-1, which constitutively produces prostaglandins and COX-2, which is induced by inflammation. Study 1. Hypothesis: A non-specific cyclooxygenase inhibitor, flunixin would retard repair of ischemic intestinal injury, whereas a selective COX-2 inhibitor, etodolac would permit repair. Equine jejunum was subjected to ischemia for 60-minutes, and recovered in Ussing chambers. In ischemic tissue treated with flunixin, production of prostaglandins was inhibited, with evidence of recovery. Untreated ischemic tissues or tissues treated with etodolac had significant elevations in prostaglandins, and significant recovery. Study 2. Hypothesis: A non-selective COX inhibitor, flunixin would retard repair of bile-injured colon, whereas the selective COX-2 inhibitor, etodolac would not inhibit repair. Equine colon was exposed to 1.5mM deoxycholate for 30-minutes, and recovered in Ussing chambers. Recovery of bile-injured colonic mucosa was not affected by flunixin or etodolac, despite significantly depressed prostaglandin production. Control tissue treated with flunixin had increases in mucosal permeability, whereas treatment with etodolac had no significant effect. Study 3. Hypothesis: Physiologic concentrations of deoxycholic acid (a bile acid) would retard repair of ischemic intestinal injury. Porcine ileum was subjected to 45-minutes of ischemia, mounted in Ussing chambers, and exposed to varying concentrations of deoxycholic acid. The ischemic episode resulted in significant damage which recovered, associated with significant reductions in mucosal permeability. Treatment of ischemic-injured tissues with 10-5 M deoxycholic acid fully inhibited recovery with significant increases in mucosal permeability, whereas 10-6M deoxycholic acid had no effect. Histology revealed complete restitution regardless of treatment, indicating the breakdown in barrier function was due to changes in paracellular permeability. Application of 10-5M taurodeoxycholic acid had similar effects. The effects of deoxycholic acid were reversed with application of the Ca2+ mobilizing agent thapsigargin. These studies show that selective COX-2 inhibitors may be advantageous in the treatment of colic and that bile may retard the repair of ischemic-injured intestine.

ISBN: 9780496553006Subjects--Topical Terms:

1017835
Biology, Animal Physiology.

The role of the enzyme cyclooxygenase and bile in the damage and repair of intestinal epithelium.
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035 $a (UnM)AAI3107752
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040 $a UnM $c UnM
100 1 $a Campbell, Nigel Brent. $3 1909570
245 1 4 $a The role of the enzyme cyclooxygenase and bile in the damage and repair of intestinal epithelium.
300 $a 164 p.
500 $a Source: Dissertation Abstracts International, Volume: 64-10, Section: B, page: 4704.
500 $a Chair: Anthony Thomas Blikslager.
502 $a Thesis (Ph.D.)--North Carolina State University, 2003.
520 $a Colic describes poorly localized abdominal pain and is treated with nonsteroidal anti-inflammatory drugs (NSAIDs). They inhibit the enzyme cyclooxygenase (COX), which has two isoforms: COX-1, which constitutively produces prostaglandins and COX-2, which is induced by inflammation. Study 1. Hypothesis: A non-specific cyclooxygenase inhibitor, flunixin would retard repair of ischemic intestinal injury, whereas a selective COX-2 inhibitor, etodolac would permit repair. Equine jejunum was subjected to ischemia for 60-minutes, and recovered in Ussing chambers. In ischemic tissue treated with flunixin, production of prostaglandins was inhibited, with evidence of recovery. Untreated ischemic tissues or tissues treated with etodolac had significant elevations in prostaglandins, and significant recovery. Study 2. Hypothesis: A non-selective COX inhibitor, flunixin would retard repair of bile-injured colon, whereas the selective COX-2 inhibitor, etodolac would not inhibit repair. Equine colon was exposed to 1.5mM deoxycholate for 30-minutes, and recovered in Ussing chambers. Recovery of bile-injured colonic mucosa was not affected by flunixin or etodolac, despite significantly depressed prostaglandin production. Control tissue treated with flunixin had increases in mucosal permeability, whereas treatment with etodolac had no significant effect. Study 3. Hypothesis: Physiologic concentrations of deoxycholic acid (a bile acid) would retard repair of ischemic intestinal injury. Porcine ileum was subjected to 45-minutes of ischemia, mounted in Ussing chambers, and exposed to varying concentrations of deoxycholic acid. The ischemic episode resulted in significant damage which recovered, associated with significant reductions in mucosal permeability. Treatment of ischemic-injured tissues with 10-5 M deoxycholic acid fully inhibited recovery with significant increases in mucosal permeability, whereas 10-6M deoxycholic acid had no effect. Histology revealed complete restitution regardless of treatment, indicating the breakdown in barrier function was due to changes in paracellular permeability. Application of 10-5M taurodeoxycholic acid had similar effects. The effects of deoxycholic acid were reversed with application of the Ca2+ mobilizing agent thapsigargin. These studies show that selective COX-2 inhibitors may be advantageous in the treatment of colic and that bile may retard the repair of ischemic-injured intestine.
590 $a School code: 0155.
650 4 $a Biology, Animal Physiology. $3 1017835
650 4 $a Biology, Veterinary Science. $3 1021733
690 $a 0433
690 $a 0778
710 2 0 $a North Carolina State University. $3 1018772
773 0 $t Dissertation Abstracts International $g 64-10B.
790 1 0 $a Blikslager, Anthony Thomas, $e advisor
790 $a 0155
791 $a Ph.D.
792 $a 2003
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