Hypercalcitoninaemia in vipomas.
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Biomedical subjects
Publications and source records attributed to H Besterman.
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The slow marker perfusion technique was used in five patients with the Zollinger-Ellison syndrome in order to determine the basal and postcibal flow rates of fluids passing the duodenojejunal junction and distal ileum, and the composition of those fluids. Fecal water and electrolyte excretions were also measured. The 24-hr outputs at the ligament of Treitz were markedly increased, while fecal losses were normal or only slightly increased. Thus, the overall intestinal reabsorption of water was 96%. Fasting rates of fluid and electrolyte flow at the ligament of Treitz were also measured during a basal period, followed by a period of continuous gastric aspiration. Removal of gastric secretion had the following effects on the fluid passing through the duodenum: (1) dramatic decrease in flow rate; (2) an increase in osmolality, from hypotonicity to isotonicity; (3) rise of pH, from acid to alkaline values; (4) a decrease of PCO2, from high to normal values. No increase in fasting plasma levels of immunoreactive secretin and motilin was observed in Zollinger-Ellison syndrome, whereas normal subjects respond to acid in the duodenum by a marked rise in the circulating levels of these hormones. These facts suggest that, in Zollinger-Ellison syndrome: (1) the ability of the small bowel and colon to reabsorb water and electrolytes is normal: (2) duodenal dissipation of hydrogen ions is mainly due to intraluminal neutralization by bicarbonate; and (3) stimulation of water and electrolyte secretion by the pancreas is inadequate.
The effects on motilin release of various stimuli including an ordinary hospital lunch and ingestion of equicaloric amounts of protein (steamed cod), fat (double cream), or carbohydrate (glucose solution), and intraduodenal instillation of acid (0.1M HCl) and alkali (0.3M tris buffer, pH 10.2) have been investigated in healthy volunteers. Duodenal acidification resulted in a 90% rise of plasma motilin while after intraduodenal instillation of alkali motilin fell. No significant change was seen after a normal hospital lunch and the protein meal, and a small fall was observed after glucose. By contrast, after ingestion of 60 g fat motilin showed a peak increase of 65% at 30 minutes and was still significantly elevated at 60 minutes. Exogenous motilin has been reported to delay gastric emptying and this is also seen after duodenal acidification and fat ingestion. We conclude that motilin may be released physiologically by these stimuli and mediate their effects on gastric emptying in man.