SUMMARY The effect of duodenogastric reflux on systemic and portal venous blood concentrations of somatostatin has been studied in the dog. Duodenogastric reflux suppressed somatostatin concentrations in both systemic and portal venous blood, but this did not occur when bile alone was diverted into the stomach. The suppression was also much less marked when truncal vagotomy accompanied the reflux. These findings suggest that altered somatostatin activity may play a part in the production of the pathophysiological changes occurring in clinical conditions such as peptic ulceration, in which there is an increase in duodenogastric reflux.Dogs with surgically produced duodenogastric reflux hypersecrete gastric acid in response to pentagastrin1 but not to histamine.2 (Table). This selective hypersecretory response is accompanied by normal fasting serum gastrin concentrations but hypergastrinaemia in response to a standard meal3 and is associated with antral gland hyperplasia.4These changes do not occur with bile diversion alone into the stomach5 and can be abolished by the addition of truncal vagotomy.6 One possible explanation of these functional changes would be that duodenogastric reflux suppresses a naturally occurring inhibitory substance produced by the antrum, that normally suppresses gastrin release from the G cells and also inhibits the acid response to pentagastrin, but not to histamine. Somatostatin fulfils these criteria and indeed a low dose infusion of 0*25 ug/kg/h has been found to restore the functional changes seen with duodenogastric reflux down to control levels.7 The effects of such reflux have therefore been studied on the systemic and portal venous concentrations of somatostatin.
Methods
ANIMALSAdult litter mate beagles were randomly allocated into four groups each of five animals.2(1) A control group. (2) A group with bile diversion, achieved by ligating and dividing the