Pharmacological inhibition of chenodeoxycholate-induced fluid and mucus secretion and mucosal injury in the rabbit colon

Michael Camilleri, R. Murphy, V. S. Chadwick

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

The effects of various pharmacological agents on bile acid-induced fluid secretion, mucus secretion, and mucosal injury were investigated using a perfusion technique in rabbit colon. Atropine markedly reduced and carbachol potentiated the fluid secretion, mucus output, and mucosal damage observed during bile acid perfusion. In contrast, pretreatment of the colonic mucosa with lignocaine and parenteral administration of methysergide and somatostatin produced a modest reduction in the fluid secretory response without apparent effects on mucus output or mucosal damage. These results suggested that cholinergic agonists and antagonists influence the mucosal resistance to bile acid-induced injury possibly through their effects on mucus secretion. Increasing or decreasing mucosal resistance to the detergent effects of bile acids appeared to have marked effects on the magnitude of induced fluid secretion. A minor reduction in overall secretory response to bile acids was also apparent with agents not influencing mucus secretion or mucosal injury.

Original languageEnglish (US)
Pages (from-to)865-869
Number of pages5
JournalDigestive Diseases and Sciences
Volume27
Issue number10
DOIs
StatePublished - Oct 1982
Externally publishedYes

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Chenodeoxycholic Acid
Fluids and Secretions
Mucus
Bile Acids and Salts
Colon
Pharmacology
Rabbits
Wounds and Injuries
Perfusion
Methysergide
Cholinergic Agonists
Cholinergic Antagonists
Carbachol
Lidocaine
Somatostatin
Atropine
Detergents
Mucous Membrane

ASJC Scopus subject areas

  • Gastroenterology

Cite this

Pharmacological inhibition of chenodeoxycholate-induced fluid and mucus secretion and mucosal injury in the rabbit colon. / Camilleri, Michael; Murphy, R.; Chadwick, V. S.

In: Digestive Diseases and Sciences, Vol. 27, No. 10, 10.1982, p. 865-869.

Research output: Contribution to journalArticle

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