Influences of the sympatho-adrenal system on gastric motility and acid secretion and on gastroduodenal bicarbonate secretion in the cat.

Abstract

Experiments were performed on acutely vagotomized cats during chloralose anaesthesia. Gastric H+ and HCO3- secretions were calculated from the pH and PCO2 in a luminal perfusate. Gastric motility was reflected by changes in hydrostatic pressure within the luminal perfusion system ('intragastric pressure'). Duodenal HCO3- secretion was monitored by pH titration in situ. Animals with an intact sympatho-adrenal system (group 1) were compared with others subjected to splanchnicotomy (group 2), adrenal gland ligation (group 3), and splanchnicotomy plus adrenal gland ligation (group 4). Basal gastric H+ secretion, as well as vagally induced H+ secretory responses, did not differ significantly between groups. Basal gastric HCO3- secretion was lower in all groups with a manipulated sympatho-adrenal system compared to the intact controls. Vagally induced increases in gastric HCO3- secretion were enhanced in the splanchnicotomized groups (groups 2 and 4). Basal as well as vagally induced increases in intragastric pressure and duodenal HCO3- secretion were enhanced in animals subjected to splanchnicotomy, with or without simultaneous adrenal gland ligation (groups 2 and 4). Adrenal gland ligation per se had no such effects. The results suggest that the adrenal glands exert a stimulatory action on basal gastric HCO3- secretion. Basal intragastric pressure and basal duodenal HCO3- secretion are inhibited by post-ganglionic sympathetic neurons, not involving the adrenal glands. Also, vagal excitatory effects on gastric motility, as well as on gastric and duodenal HCO3- secretions, are inhibited by such a direct neural mechanism.