High systemic HCO3(-) and topical 16,16-dimethyl-PGE2 protect gastric mucosa against luminal acid by enhancing its preepithelial buffer capacity.

Systemic metabolic alkalosis and topical prostaglandins protect the gastric mucosa against luminal acid. This study investigates whether this protection is mediated by increased epithelial HCO3(-) secretion with resultant alkalization of the pre-epithelial mucus-HCO3(-) buffer layer. surface pH of chambered ex vivo rat gastric epithelium was measured with liquid sensor pH microelectrodes during luminal perfusion of increasing acidities (0, 10, 30, 50, 100 mM HCL). The experimental groups were: (1) control, (2) topical 16,16-dimethyl-PGE2 treatment, (3) high-HCO3(-) metabolic alkalosis, and (4) low HCO3(-) respiratory alkalosis. The gastric mucosa of PGE2-treated and high-HCO3(-) alkalotic rats tolerated significantly better luminal acid than that of controls, but the tolerance of low-HCO3(-) alkalotic rats was significantly impaired. There was a significant correlation between arterial HCO3(-) concentration (but not arterial pH) and surface pH (r = 0.81, P < 0.01). This suggests that the gastric mucosa against luminal acid are, at least in part, mediated by enhanced buffer capacity of the pre-epithelial mucus-HCO3(-)layer.