Anti-stress ulcer and anti-secretory effect of somatostatin in rats -- failure to suppress serum gastrin.

In rats the influence of arresting free motions (= controls; mild stress) and of restraint (= severe stress) without and with additional somatostatin (SRIF) on gastric secretion, mucosal microcirculation and stress ulcer formation was studied. Severe stress alone reduces volume, acid and pepsin secretion, acid concentration, aminopyrine clearance and ratio. The ulcer index is elevated. Under both conditions SRIF inhibits in a dose-dependent manner volume and acid secretion, and ulcer incidence is lower. The interaction between severe stress and the antiulcer component of SRIF is characterized as non-competitive. Under these conditions and a continuous infusion of SRIF (10.0 microgram/kg.h over 8 h) acid concentration, acid and pepsin secretion fall subtotally, ulcer index to 50 percent of vehicle (saline) treated rats, if gastric fistula drains juice outside stomach. Microcirculation and serum gastrin are unchanged. In animals with closed fistula ulcer index is reduced by 85 percent, average gastrin again is unchanged. It is concluded that stress ulcers develop at a low secretory and microcirculatory state of gastric mucosa. The prophylactic effect of SRIF results from direct inhibition of parietal and chief cells and additional yet unknown factors.