Abstract
The possibility that the gut peptide, neurotensin, may contribute to the dumping syndrome was investigated in 17 patients with a long history of dumping after a Billroth II gastrectomy for duodenal ulcer. After a test meal plasma levels of neurotensin were higher than in normal subjects, but no correlation to the severity of symptoms was found. In eight of the patients with meal-provoked dumping symptoms, intravenous infusion of neurotensin in relevant doses produced neither symptoms nor changes in blood glucose, blood pressure, or pulse rate. The apparent plasma half-life of neurotensin (t1 = 2.3 min) did not differ from that previously found in normal subjects. The results indicate that it is unlikely that neurotensin alone has a pathogenetic role in the dumping syndrome in gastrectomized patients.
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