Abstract
Chloralosed cats were acutely vagotomized, their splanchnic nerves cut and the adrenal glands ligated. The gastric lumen was perfused with isotonic NaCl and gastric motility was monitored as changes in hydrostatic pressure within the perfusion circuit. Gastric secretion of H+ HCO3 were calculated from continuous measurements of pH and Pco2 Methodological tests ex vivo showed good accuracy of the estimations. Recovery of H+ after HCl instillation into the stomach in vivo was almost complete, while HCO3 recovery after NaHCO3 instillatons was 85–95%. Pentagastrin (10μg kg‐1 h‐1 i.v.) stimulated gastric contractile activity and increased gastric H+ secretion 30‐fold, while HCO3 secretion decreased somewhat. Carbachol (4μg kg‐1 h‐1) induced gastric contractions and increased H+ secretion by 400% and HCO3 output by 100–130%. Electrical stimulation of the cut vagal nerves (10 Hz for 10 min) induced well known gastric motor responses and increased gastric H+ secretion 20‐fold preceded By a transient doubling of HCO3 secretion. Omeprazole, a selective inhibitor of gastric H+ secretion, decreased the vagally induced H+ secretion, while recorded gastric HCO3 secretion was clearly enhanced. In conclusion, the technique permits simultaneous recordings of rapid alterations of gastric motility and H+ HCO3 secretions. However, HCO3 secretion was modestly underestimated, probably due to mucosal CO2 absorption.