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BILE SALT‐INDUCED INJURY OF RABBIT OESOPHAGEAL MUCOSA MEASURED BY HYDROGEN ION DISAPPEARANCE
Author(s) -
Kiroff GeorgeK.,
Devitt PeterG.,
Deyoung NevilleJ.,
Jamieson GlynG.
Publication year - 1987
Publication title -
australian and new zealand journal of surgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.111
H-Index - 51
eISSN - 1445-2197
pISSN - 0004-8682
DOI - 10.1111/j.1445-2197.1987.tb01314.x
Subject(s) - hydrochloric acid , medicine , salt (chemistry) , gastroenterology , bile acid , micelle , reflux , sodium , perfusion , taurocholic acid , chemistry , inorganic chemistry , aqueous solution , disease , organic chemistry
Oesophageal injury secondary to gastro‐oesophageal reflux is unlikely to be due to the effects of hydrochloric acid alone. The present authors have investigated the development of acid and bile salt‐induced oesophageal mucosal injury in a rabbit model. Solutions of hydrochloric acid and sodium taurocholate (st) were perfused through an isolated oesophageal preparation and mucosal injury was determined by measuring the rate of h + disappearance. Perfusion with acid alone in concentrations up to 10 mmol/1 did not affect the h + disappearance rate. Addition of 1 mmol/1 st to an acid perfusate resulted in loss of h + from the system. The increase in h + disappearance rate was associated with loss of st from the perfusate. Sodium taurocholate was only lost from the system when in an acid medium. Increased rate of h + disappearance occurred even after the bile salt had been washed out of the perfused oesophagus. The mechanism of bile salt‐induced mucosal injury was unlikely to be due to mucosal disruption secondary to micelle formation since the critical micellar concentration of taurocholate was found to be greater than that used in the perfusate. These findings indicate that bile salts may be an important factor in hydrochloric acid‐related damage to oesophageal mucosa, by acting through mechanisms unrelated to micelle formation.