Arteriovenous acid-base balance during acute gastric mucosal ulcerogenesis.
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.
D000136:Acid-Base Equilibrium; D000818:Animals; D001639:Bicarbonates / Q000097:blood; D004285:Dogs; D005260:Female; D006863:Hydrogen-Ion Concentration; D008297:Male; D013276:Stomach Ulcer / Q000097:blood*
D001639:Bicarbonates