The action of (Gln4)-neurotensin was studied on the spontaneous motor activity in isolated canine fundic, antral and intestinal pouches. All pouches had been prepared more than 6 months prior to the experiments. Spontaneous motor activity was recorded for at least 1 h before the Gln4)-neurotensin was infused i.v. for 30 min in doses ranging between 6.3 and 100 ng X kg-1 X min-1. In the vagally denervated fundic pouches (Gln4)-neurotensin inhibted motor activity in doses above 25 ng X kg-1 X min-1. The vagally innervated antral pouches were more sentitive than the vagally denervated fundic pouches to the action of (Gln4)-neurotensin. Thus motor inhibition was induced by doses as low as 6.3 ng X kg-1 X min-1. The effect of (Gln4)-neurotensin on motor activity in intestinal pouches was inconsistent. Inhibition was seen in 1 out of 7 expts. The present results show that the gastric motor activity is the most sensitive function to (Gln4)-neurotensin so far studied.
In 6 patients having duodenal ulcer disease plasma gastrin concentrations were determined before and after the oral administration of 0.5-2 g of calcium carbonate, 2-4 tablets of Carnalox@ and 2 tablets of NovalucoP. No significant influence on basal plasma gastrin levels was noted indicating that antacids, whether they contain calcium carbonate or not, do not influence the basal plasma concentration ofgastrin at occasional administration.
The intra-operative surface pH of the corpus fundic mucosa in anaesthetized dogs was studied with a glass electrode during stimulation with graded doses of pentagastrin. The mucosal pH could be related to the dose of pentagastrin by a hyperbolic curve. With intact vagus ED50 averaged 0.67 micrograms kg-1 h-1 of pentagastrin and maximum effect corresponded to an average pH of 1.9. Immediately after truncal vagotomy there was a significant shift of the curve to the right corresponding to an average ED50 of 3.77 micrograms kg-1 h-1, an effect that could be described as that of a competitive inhibitor. Two weeks after vagotomy the value of ED50 had returned to the prevagotomy level. The high ED50 immediately after vagotomy is ascribed to the sudden fall in the subthreshold release of acetylcholine previously supplied by the intact vagus. The return to the low ED50 2 weeks later could be explained by denervation supersensitivity. The relation between the curves before and immediately after vagotomy suggests that the dose of the agonist be as low as possible, when testing the completeness of a vagotomy intra-operatively.
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