SUMMARY Serum gastrin concentrations were measured in patients with duodenal ulcer and controls before, during, and after one-hour intravenous infusion of various doses of adrenaline (0-12 jig to 6 ,ug/min). Gastrin concentrations in the basal state were significantly increased in duodenal ulcer patients compared to controls. The maximal rise in serum gastrin concentrations was obtained at a dose of 4 ,ug/min adrenaline in both groups of subjects, and the increase was significantly higher in duodenal ulcer patients than in controls. Adrenaline increased predominantly the gastrin III component (gastrin-17 like) in both duodenal ulcer patients and controls. The threshold level of adrenaline-induced gastrin release was significantly lower in duodenal ulcer patients: intravenous infusion of adrenaline in a dose of 0 12 ,ug and 0-25 jig/min increased serum gastrin concentrations 23 and 43 %, respectively, but had no effect in controls. Rises in plasma adrenaline concentrations were similar in both groups of subjects in response to the various doses of adrenaline employed. Only the smallest dose of adrenaline (0-12 ug/min) resulted in clearly physiological variations in plasma adrenaline concentrations. The results indicate that endogenous adrenaline may stimulate the secretion of gastrin during physiological conditions in patients with duodenal ulcer.Adrenaline stimulates the secretion of gastrin in man and is at least partially responsible for the rise in serum gastrin concentrations during hypoglycaemia (Hayes et al., 1972;Stadil and Rehfeld, 1973;Kronborg et al., 1974;Brandsborg et al., 1975;Kaess et al., 1975).Previous studies have demonstrated a relationship between plasma adrenaline and serum gastrin concentrations during hypoglycaemia as well as between intravenous infusion of adrenaline and rise in serum gastrin (Stadil and Rehfeld, 1973;Brandsborg et al., 1975;Christensen and Stadil, 1976 10 October 1977 in control subjects .The present study concerns the interrelationship between intravenous infusion of adrenaline, plasma adrenaline concentration, and serum gastrin in patients with duodenal ulcer and controls. Methods SUBJECTS AND PROCEDURETwenty-one normal male subjects (mean age 34 years, range 25-47 years) and 19 male patients (mean age 38 years, range 26-51 years) with radiologically verified non-obstructing duodenal ulcer participated in 35 and 40 infusion experiments, respectively. An informed consent to the procedure was obtained from all subjects examined.The study was performed in the morning with subjects resting in the supine position after an overnight fast. Adrenaline was infused intravenously for one hour in both groups of subjects in the following doses: 0X25 ,ug/min, 1 ,tg/min, 2 ,tg/min, 4 ,tg/min, and 6 ,ug/min. A dose of 0X12 ,ug/min for one hour was given to the duodenal ulcer patients only. Each dose of adrenaline was given to six to 202

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Intravenous infusion of isoproterenol, a beta-adrenergic receptor stimulatory agent, increased serum gastrin concentration significantly more in patients with a duodenal ulcer than in healthy subjects. The rise in pulse rate, blood glucose concentration and in serum insulin was the same in both groups of subjects. Gastrin secretion was also increased significantly more in the patients than in the control subjects after a beef-meal. Basal serum gastrin concentrations were higher in the patients than in the control subjects and correlated to the rise in serum gastrin during both tests in the patients with a duodenal ulcer. Isoproterenol and meal stimulated gastrin secretion, expressed as percent of the basal value, were twice as higher in the patients as in the control subjects. The combined administration of isoproterenol and the meal had an additive effect on the rise in serum gastrin. Isoproterenol stimulated gastrin secretion was completely suppressed by propranolol, a beta-adrenergic receptor blocking agent, which had no effect on meal stimulated gastrin secretion. It is concluded that the mechanism of the hypersecretion of gastrin in patients with a duodenal ulcer did not involve a specific abnormality of the beta-adrenergic receptor or the receptor which recognized proteins and their digested products. There is no established role of beta-adrenergic receptor activity in the hypersecretion of gastrin in patients with duodenal ulcers. It is suggested that the beta-adrenergic receptor may have some yet unknown function unrelated to the acute secretory response of gastrin.

The low-dose oral iron absorption test (OIAT), a possible test for iron deficiency, is based on the fact that intestinal iron absorption is higher in iron-deficient subjects than in those with normal or increased iron stores. The aims of this study were to establish a reference interval for the OIAT, to evaluate five different ways of presenting the results, and to advocate for the use of one of these methods. OIAT was performed in 122 healthy volunteers, 3 of whom were excluded as a result of technical difficulties. The volunteers were given 10 mg of oral iron sulphate at 0900 h on an empty stomach. S-iron was measured just before iron consumption, and after 1, 2 and 3 h. The maximum increase in S-iron during the test, presented as Cmax (micromol l(-1)), was higher in females (5 [median]; 3 and 7 [1st and 3rd quartiles]; 0-34 [range]) than in males (3; 1 and 5; 0-13) (p<0.001 Mann Whitney U-test). Furthermore, Cmax was significantly higher in females aged 22 44 years than in all other age groups (males and females), but did not fluctuate significantly with age in males. Cmax was higher in premenopausal than in postmenopausal females (6; 5 and 10; 0-34 and 4; 2 and 5; 0-12, respectively) (p <0.01 Mann Whitney U-test). In conclusion, iron absorption assessed by the OIAT was higher in premenopausal females than in postmenopausal females and males. We suggest reference intervals of 0-34 micromol l(-1) in premenopausal females, and 0-11 micromol l(-1) in all other persons, i.e. males and postmenopausal females.