Bile acid-induced acute gastric mucosal damage: a useful experimental model.
A model was developed to assess the influence of the bile acids on the ability of proximal gastric mucosa to maintain electrical and pH gradients and to resist acute morphologic injury. It was found that the combination of topical acid, topical bile acid, and mucosal ischemia is acutely and severely ulcerogenic. Lesion severity is a function of the absolute amount of H+ diffusing into the mucosa which is, itself, a function of the intraluminal concentrations of both bile acid and H+. Morphologic injury is associated with the development of a marked gastric venous acidosis. Bile acid species differ in their capacity to induce lesions. Topical application of bile acids to non-ischemic mucosa is not acutely ulcerogenic because of a compensatory increase in mucosal blood flow occurs which is proportional to the degree of H+ loss induced. In the present model, steroids are cytoprotective by virtue of this mechanism, while H1 and H2 blocking agents, either alone or in combination, are not. Prostaglandins are also cytoprotective but by mechanisms which do not involve altered mucosal blood flow.
D000818:Animals; D001647:Bile Acids and Salts / Q000502:physiology*; D001655:Bile Reflux; D004285:Dogs; D005753:Gastric Mucosa / Q000098:blood supply; D006863:Hydrogen-Ion Concentration; D007511:Ischemia / Q000209:etiology; D008954:Models, Biological; D013276:Stomach Ulcer / Q000209:etiology*
D001647:Bile Acids and Salts