Effects of acute administration of omeprazole or ranitidine on basal and vagally stimulated gastric acid secretion and alkalinization of the duodenum in anaesthetized cats

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Abstract
Experiments were performed on acutely vagotomized cats during chloralose anaesthesia. In order to avoid sympathoadrenergic influences, the adrenal glands were ligated and the splanchnic nerves were cut bilaterally in all animals. The gastric lumen was perfused with saline and the H+ secretion was caculated from pH measurements in the perfusate. HCO3- secretion by the duodenal mucosa was titrated in situ. Omeprazole (4 mg kg-1 i.v., dissolved in PEG400, 40% w/v) did not influence basal or vagally induced HCO3- secretions, but inhibited by about 80% the H+ secretory response induced by electric vagal stimulation. Acute administration of ranitidine (5 mg kg-1 i.v.) transiently lowered arterial pressure, an effect which was followed by a sustained compensatory tachycardia. Ranitidine raised basal duodenal HCO3- secretion by 50% and inhibited vagally induced gastric H+ secretion by about 70%, whereas vagally induced HCO3- secretion was not influenced. The results suggest that vagal nerve stimulation raises the duodenal bicarbonate secretion via a mechanism independent of the level of gastric H+ secretion.