| pubmed-article:6312193 | pubmed:abstractText | Recent studies suggest that HCO-3 production by surface epithelium may protect gastric mucosa against H+ back diffusion. Agents shown to increase gastric HCO-3 include prostaglandins, carbachol, dibutyryl c-GMP, ethanol, Ca2+, and cimetidine. This study was initiated to evaluate the effect of secretin on gastric mucosal HCO-3 production. Six dogs with Heidenhain pouches were fasted 24 hr. Each study consisted of nine 15-min periods: three control periods of iv saline infusion; three test periods which followed an iv bolus of 0.15 clin units/kg secretin; and three test periods which followed an iv bolus of 0.30 clin units/kg secretin. The intragastric test solution consisted of 100 mM NaCl, 20 mM mannitol, and 50 mM EPPS buffer; pH was adjusted to 8.0-8.2 using 19 M NaOH. Fifty milliliters test solution was instilled in the pouch and a zero-time sample was taken; after 15 min a final sample was taken, the pouch was rinsed, and the next period begun. HCO-3, Na+, K+, and Cl- concentrations were measured as well as transmucosal electrical potential difference (PD) changes and changes in volume, pH, and osmolality. [14C]PEG was utilized to measure residual volume. In the first 15-min period following each secretin bolus, significant (P less than 0.05) increases in intraluminal gastric HCO-3 occurred. However, doubling the secretin dose did not significantly increase the measured HCO-3 when compared to the lower dose. Also undetectable were changes in ionic fluxes accompanying the increases in intraluminal HCO-3 which might have suggested a mechanism of the HCO-3 production. In addition to its previously described properties of acid inhibition and gastric mucus stimulation, this study demonstrates that secretin also induces production of gastric HCO-3.(ABSTRACT TRUNCATED AT 250 WORDS) | lld:pubmed |
