Influence of acid secretory state on the gastric mucosal tolerance to back diffusion of H+.
The effect of back diffusion of H+ PON THE POTENTIAL DIFFERence (PD), electrical resistance (R), and short circuit current (Isc) of spontaneously secreting and burimamide-inhibited amphibian gastric mucosae were studied in vitro. When back diffusion of H+ was induced by the passage of an electrical current of 510 mua per cm2 from the secretory (S) side of pH 2.25 to the nutrient side (N) for 30 min, the spontaneously secreting mucosae showed small decreases in PD (23.6 leads to 16.2 mv) and Isc (80 leads to 61 mua per cm2) but no significant change in R. In the burimamide-inhibited mucosae there were marked and significantly greater decreases of PD (26.8 leads to 3.4 mv), R (473 leads to 170 ohms cm2) and Isc (50 leads to 13 mua per cm2). When back diffusion of H+ was induced by establishing a concentration gradient of H+ from S leads to N or by exposing the secretory surface to sodium taurocholate with secretory pH 2.25, the burimamide-inhibited tissue demonstrated significantly greater depression of the electrical parameters than the secreting mucosae. Intracellular pH, measured by the 5,5-dimethoxyazolidine-2,4-dione method, was significantly higher in the histamine-stimulated tissues (7.28) than in the metiamide-inhibited tissues (7.11). These studies strongly suggest that the secretory status of the mucosa and hence its acid-base status are important determinants in the tolerance of the tissue to exogenous back diffusion of H+. The measure of absolute loss of H+ From the mucosal solution alone may not be an adequate assessment of the gastric mucosal barrier.
Influence of acid secretory state on the gastric mucosal tolerance to back diffusion of H+. The effect of back diffusion of H+ PON THE POTENTIAL DIFFERence (PD), electrical resistance (R), and short circuit current (Isc) of spontaneously secreting and burimamide-inhibited amphibian gastric mucosae were studied in vitro. When back diffusion of H+ was induced by the passage of an electrical current of 510 mua per cm2 from the secretory (S) side of pH 2.25 to the nutrient side (N) for 30 min, the spontaneously secreting mucosae showed small decreases in PD (23.6 leads to 16.2 mv) and Isc (80 leads to 61 mua per cm2) but no significant change in R. In the burimamide-inhibited mucosae there were marked and significantly greater decreases of PD (26.8 leads to 3.4 mv), R (473 leads to 170 ohms cm2) and Isc (50 leads to 13 mua per cm2). When back diffusion of H+ was induced by establishing a concentration gradient of H+ from S leads to N or by exposing the secretory surface to sodium taurocholate with secretory pH 2.25, the burimamide-inhibited tissue demonstrated significantly greater depression of the electrical parameters than the secreting mucosae. Intracellular pH, measured by the 5,5-dimethoxyazolidine-2,4-dione method, was significantly higher in the histamine-stimulated tissues (7.28) than in the metiamide-inhibited tissues (7.11). These studies strongly suggest that the secretory status of the mucosa and hence its acid-base status are important determinants in the tolerance of the tissue to exogenous back diffusion of H+. The measure of absolute loss of H+ From the mucosal solution alone may not be an adequate assessment of the gastric mucosal barrier.