Effects of monoclonal antibodies to somatostatin on somatostatin-induced and intestinal fat-induced inhibition of gastric acid secretion in the rat.

Cell lines producing monoclonal antibodies to somatostatin, designated S10 and S20, have recently been generated. The purpose of the present immunoneutralization study was to examine the ability of these antibodies to block the inhibitory effect of exogenous somatostatin on meal-stimulated gastric acid secretion in the innervated rat stomach and to use these antibodies as probes to determine if somatostatin is involved in intestinal fat-induced inhibition of gastric acid secretion. The plateau acid secretory response to a liver extract meal in this model was 28 +/- 2 mu Eq/30 min. Intravenous infusion of somatostatin at 2.0 micrograms/kg X h or intraduodenal oleic acid at 1.2 ml/h reduced this response to 12 +/- 1 and 14 +/- 1 mu Eq/30 min, respectively. The antibodies were given intravenously 1 h before the meal and either somatostatin or intraduodenal oleic acid infusion. S10 preinfusion returned the plateau meal responses to the levels seen with the meal alone: 25 +/- 4 and 26 +/- 1 mu Eq/30 min, respectively. S20 preinfusion had no effect, the responses being 14 +/- 1 and 16 +/- 1 mu Eq/30 min, respectively. These results demonstrate successful binding of exogenous somatostatin by S10 in vivo and reversal of intestinal fat-induced inhibition of gastric acid secretion by S10 preinfusion. It is concluded that the mechanism whereby fat in the small intestine inhibits gastric acid secretion may involve the release of somatostatin.