Serum gastrin level and gastric somatostatin content and binding in long-term pyloromyotomized children

Abstract

Since somatostatin inhibits basal and stimulated gastric acid secretion and gastrin release, it is conceivable that decreased gastric somatostatin concentration may be one of the factors responsible for gastric hypersecretion found in patients who have undergone long-term pylorotomy for hypertrophic pyloric stenosis. To investigate this proposal the somatostatin-like immunoreactivity concentration was determined in antral and fundic mucosa samples from control and long-term pyloromyotomized children. In addition, somatostatin binding to cytosol from gastric (fundus and antrum) mucosa and fasting serum gastrin levels and serum gastrin response to a standard breakfast were also studied. The mean fundic and antral somatostatin-like immunoreactivity concentrations were significantly lower in long-term pyloromyotomized children than in control children. The depletion of fundic and antral somatostatin-like immunoreactivity content was associated with an increase in the number of gastric somatostatin binding sites. The fasting serum gastrin levels and serum gastrin response to a standard breakfast (after 60 min) in long-term pyloromyotomized children was significantly higher than those in control children. Since, together with the increase of somatostatin binding to gastric mucosa, there is an increase in the gastrin serum levels, despite the inhibitory effect of somatostatin on gastrin release, the binding capacity cannot be the main factor determining the response to somatostatin in long-term pyloromyotomized children. The present results suggest that both somatostatin and gastrin have some pathophysiologic importance in long-term pyloromyotomized children.