Anesthetic dependence of the inhibitory effect of neurotensin on pentagastrin-stimulated acid secretion in rats. A possible role for somatostatin.
ABSTRACT The existence of possible local mediators of the inhibitory effect of neurotensin on gastric acid secretion has not been determined. We perfused rats intragastrically with warmed saline and stimulated acid secretion with intravenous pentagastrin, 32 micrograms/kg/hr, and found that anesthesia with pentobarbital resulted in marked inhibition of acid secretion by intravenous neurotensin; however, anesthesia with urethane prevented this inhibitory effect of neurotensin from occurring. In addition, we found a significant increase in somatostatin-like immunoreactivity in portal venous blood during neurotensin infusion in pentobarbital-anesthetized rats. Neither neurotensin nor pentagastrin infusion modified gastric luminal somatostatin-like immunoreactivity after either pentobarbital or urethane, and rats anesthetized with urethane did not show an increase of somatostatin-like immunoreactivity in portal venous blood during neurotensin infusion. These results suggested that somatostatin-like immunoreactivity, released into the portal circulation, was necessary for exogenous neurotensin to inhibit pentagastrin-stimulated gastric acid secretion under these conditions in anesthetized rats.
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ABSTRACT: Anaesthetic agents affect gastric acid secretion, but the mechanisms behind this action have not been fully evaluated. The enterochromaffin-like (ECL) cell plays a key role in the regulation of gastric acid secretion, and anaesthetic agents have recently been described as inhibiting histamine release from the ECL cell. The present study examines the effect of anaesthetic agents on the ECL cell and on parietal cell functions. Different concentrations of urethane, pentobarbital and a mixture of fluanisone/fantanyl/midazolam (FFM) were examined for the effect on gastrin-stimulated histamine release and acid secretion and on histamine-stimulated acid secretion in the totally isolated vascularly perfused rat stomach. The luminal acid output and histamine concentrations in venous effluents were measured by titration and radioimmunoassay, respectively. Pentobarbital caused an inhibition on both histamine release and acid output in gastrin-stimulated stomachs in a concentration-dependent way. The mixture of FFM at higher concentrations inhibited histamine release from the ECL cell and luminal H+ output in gastrin-stimulated acid secretion. Urethane exerted a slight inhibitory effect on histamine release only at the lowest concentration. Pentobarbital also reduced histamine-stimulated gastric acid secretion, while the mixture of FFM did not. pentobarbital inhibits acid secretion both by reducing ECL cell histamine release and parietal cell H+ secretion, whereas FFM inhibits acid secretion by interaction with the ECL cell only. Urethane also had a slight inhibitory effect on the ECL cell histamine release at the lowest concentration.Scandinavian Journal of Gastroenterology 08/2002; 37(7):750-3. · 2.33 Impact Factor