| pubmed-article:6778760 | pubmed:abstractText | The mechanism of acute ulceration and the nature of mucosal protective mechanisms were investigated in rabbit antrum, which is more resistant to injury than fundus of the same species, with particular reference to the relationship between H+ back diffusion, tissue acidification, and occurrence of ulceration. Exposure of antral pouches to increasing luminal [H+] during short-term hemorrhagic shock caused progressive acidification of the mucosa as measured by a microelectrode in the lamina propria, but ulceration of the mucosa did not occur unless an unphysiologically high [H+] (225 mM) was used. Addition of exogenous pepsin to a luminal [H+] of 80 mM increased the rate of H+ back diffusion and the degree of mucosal acidification, but ulcerations did not develop, suggesting that endogenous pepsin does not account for the ulceration of fundic mucosa under the same experimental situation. In contrast, addition of sodium taurocholate (5 mM) to the same luminal [H+] (80 mM) produced ulcerations and increased the rate of H+ back diffusion. Systemic administration of acetazolamide, an inhibitor of carbonic anhydrase, enhanced the development of ulceration without increasing the rate of back diffusion or the degree of tissue acidification. The results suggest that rabbit antral mucosa is protected from excessive acidification and ulceration by its relative impermeability to H+. When the rate of H+ back diffusion is artificially augmented to a level encountered in the fundus in an ulcerogenic situation, profound acidification with ulcerogenic situation, profound acidification with ulceration also occurs in the antral mucosa. The data also suggest that carbonic anhydrase, an enzyme abundantly present in gastric mucosa, may have a protective function in the mucosa, possibly by contributing to the regulation of intracellular pH and/or to the maintenance of mucosal HCO3- secretion. | lld:pubmed |
