Role of bile acid reflux in acute hemorrhagic gastritis

Abstract

A model was developed to assess the influence of bile acids on the ability of proximal canine gastric mucosa to maintain an intraluminal pH gradient 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 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 nonischemic mucosa is not acutely ulcerogenic because 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 histamine H1 and H2 receptor antagonists, either along or in combination, are not. The clinical applicability of these findings is discussed.

Gastric Stress Ulcer of the Rat: Relative Contribution of the Pyloric Sphincter, HCO^–₃ Bile Reflux and Mucosal Blood Flow

“…The infu sion has doubtlessly rehydrated the rats, but above all it has exercised an antacid function. Despite the different experimental condi tions, our conclusions partially confirm those of Ritchie [25], in whose opinion the increase in mucosal blood flow is proportional to the secretion of hydrogen ions by the gastric mu cosa attacked by bile. His measurements of blood flow were only carried out at the 15th and the 30th minute.…”

“…We thus agree with Rees and Bowen [24] who were able to obtain an exper imental ulcer only with a combination of bile and hydrochloric acid. This is also in agree ment with the opinion of Ritchie [25], who considers that the development of gastric ul cers results from a combination of three fac tors: ischemia, acidity and bile. The presence of one or even two of these factors is insuffi cient to give rise to a mucosal lesion [24,25,28].…”

“…This is also in agree ment with the opinion of Ritchie [25], who considers that the development of gastric ul cers results from a combination of three fac tors: ischemia, acidity and bile. The presence of one or even two of these factors is insuffi cient to give rise to a mucosal lesion [24,25,28]. The increase in the diffusion of hydrogen ion concentrations is a linear function of the concentration of the bile acids and in the case of taurocholic acid, the sole inhibitor of car bonic anhydrase [18].…”

“…The favorable effect of H C 03 ions in the prevention of acute gastric ulceration is well known [25,28,30,31]. More precisely, the presence of these ions at high concentrations allows repair of the mucosa even at an intra gastric pH of 3 [31 ].…”

Stress Ulceration: The Enigma Continues

“…However, this barrier can be disrupted by various compounds, e.g. bile salts [18], and when this occurs the hydrogen ion back diffusion markedly increases, intramural pH falls and mucosal damage ensues.…”