Sympatho‐adrenergic inhibition of vagaliy induced gastric motility and gastroduodenal HCO3‐ secretion in the cat

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Abstract
Chloralosed cats were acutely vagotomized and their adrenal glands were ligated. The gastric lumen was perfused with isotonic NaCl and gastric motility was recorded as change in hydrostatic pressure within the perfusion circuit. Gastric secretions of H+ HCO3‐ were calculated from continuous measurements of pH and pCO2 in the perfusate. Mucosal HCO3‐ secretion in the distal duodenum was titrated in situ by pH‐stat equipment. The experiments were divided into three different groups dependent on the state of sympathetic splanchnic nervous supply: (1) intact; (2) cut on a preganglionic level; (3) blocked with the adrenolytic agent guanethidine. Basal levels for gastric motility, gastric H+ HCO3‐ secretions and duodenal HCO3‐ secretion were more or less similar in all groups. Gastric motility, gastric HCO3‐ duodenal HCO3‐ secretory responses to bilateral vagal stimulation were significantly enhanced in splanchnicotom‐ized or guanethidine‐treated animals as compared to controls with intact sympathetic supply. However, no clear differences in gastric H+ secretory responses to vagal stimulation were demonstrated between animals with an intact or disrupted sympathetic innervation. These results suggest a sympatho‐adrenergic inhibitory action on vagaliy induced mucosa‐protective HCO3‐ secretion in the stomach and the duodenum. Furthermore, vagal stimulation in animals with intact splanchnic nerves induced a guanethidine‐resistant delayed increase in duodenal HCO3‐ secretion. The nature of this response was not further analysed.