Arteriovenous acid-base balance during acute gastric mucosal ulcerogenesis

Abstract

The possibility that acute gastric mucosal ulcerogenesis induced by bile acid and ischemia is a consequence of inadequate tissue buffering of back-diffused intramucosal H+ was examined indirectly by measuring arteriovenous differences in acid-base parameters across vascularized chambered wedges of proximal canine gastric wall. During acute lesion formation gastric venous [HCO3-] and pH were significantly decreased, and a marked negative base excess developed. The data suggest that mucosal ulcerogenesis is a consequence of uncompensated tissue acidosis. Further, these derangements occur only in the presence of topical acid, suggesting that back-diffused H+ may be ultimately responsible.