Abstract
The present studies were directed toward examining the effect of somatostatin on gastrin release and acid secretion by the isolated vascularly perfused rat stomach. Rat stomachs were perfused in situ with Krebs-Ringer bicarbonate buffer containing 10% ovine erythrocytes and gassed with 95% O2-5% CO2. Inclusion of pentagastrin in the perfusion buffer increased acid output from 2.2 +/- 0.4 microEq H+/h during control perfusion to 18.8 +/- 1.8 microEq H+/h (p less than 0.01). In order to determine the effect of somatostatin on acid secretion and gastrin release, specific antibodies to somatostatin were included in the perfusate. Inclusion of antibodies to somatostatin in the buffer without pentagastrin did not significantly enhance acid output; however, gastrin concentration in the portal venous effluent increased from 15.1 +/- 2.0 to 25.2 +/- 5.2 pg/ml at 45 min (p less than 0.05). When antibodies to somatostatin were perfused in the presence of pentagastrin, acid output increased by 32% to 24.9 +/- 1.2 microEq H+/h (p less than 0.05); however, no change in gastrin concentration over basal was detected in the portal effluent. Results of these studies indicate that the capacity of the isolated rat stomach to secrete acid permits direct assessment of factors involved in the regulation of acid secretion. Under the conditions of these experiments, gastric somatostatin inhibits basal gastrin release and directly inhibits pentagastrin-stimulated acid secretion without affecting gastrin release.
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