Abstract. Plasma catecholamine concentrations (PCA) were measured during standing and exercise using a precise and sensitive double‐isotope derivative technique. By plotting the increase in PCA in the standing position on the y‐axis of a coordinate system against the increase in pulse rate, PCA was resolved into two components: one corresponding to the intercept of the y‐axis where rise in pulse rate equals zero (CAP) while the other (CAH) was calculated by multiplying the slope of the regression line by the mean increase in pulse rate.–The rise in PCA, mainly noradrenaline, was considerably less during light to moderate exercise than during standing. Thus there was no rise in PCA during exercise until the increase in pulse rate exceeded approximately 30 beats/min and there was no rise in the CAP component during exercise. When PCA began to rise during exercise the increase in PCA per increment in pulse rate was similar to that observed in the standing experiments. There was no difference between the increments in PCA observed during exercise in the supine and the sitting positions but resting PCA was doubled in the sitting position.–It is suggested that 1. the initial rise in pulse rate during exercise is due to withdrawal of parasympathetic activity on the heart 2. the increase adrenergic in vasoconstrictor activity is considerably less during moderate exercise than during standing 3. the increase in plasma noradrenaline during moderate exercise is of cardiac origin.

Abstract. Plasma adrenaline‐blood glucose interrelationships in insulin‐induced hypoglycaemia in man have been studied using a sensitive double‐isotope derivative method for adrenaline estimation. Plasma adrenaline reached a peak of 1.24 ng/ml at 45 minutes after insulin while blood glucose reached a nadir of 22 mg/100 ml at 30 minutes. There was a strong correlation both between the rise in adrenaline and the degree of hypoglycaemia and between the rise in adrenaline and the post‐hypoglycaemic rise in glucose. Plasma noradrenaline rose from 0.29 to 0.59 ng/ml, the rise correlating with the rise in adrenaline. Changes in pulse rate preceded and were unrelated to changes in plasma catecholamines. Fuel mobilisation in response to adrenaline infusion (6 μg/min. for 20 min.) in normoglycaemic man was also studied. Plasma adrenaline concentration rose from a mean of 0.02 ng/ml to 0.71 ng/ml while plasma noradrenaline concentration was unchanged. Blood glucose rose from 71 to 98 mg/100 ml while plasma insulin decreased from 11 to 8 μ/ml. Blood lactate rose by 0.85 mM while pyruvate concentration remained unchanged. Blood glycerol concentration rose twofold and ketone body concentration threefold but there was little change in the concentrations of the glucogenic amino acids, alanine, glutamate and glutamine. Both the 3‐hydroxybutyrate/acetoacetate ratio and the lactate/pyruvate ratio rose implying a more reduced intracellular state due presumably to increased hepatic fatty acid oxidation. It is concluded that adrenaline enhances the recycling of lactate and spares glucose through the mobilitsation of lipids but that amino acids are little affected.

Plasma adrenaline-blood glucose interrelationships in insulin-induced hypoglycaemia in man have been studied using a sensitive double-isotope derivative method for adrenaline estimation. Plasma adrenaline reached a peak of 1.24 ng/ml at 45 minutes after insulin while blood glucose reached a nadir of 22 mg/100 ml at 30 minutes. There was a strong correlation both between the rise in adrenaline and the degree of hypoglycaemia and between the rise in adrenaline and the post-hypoglycaemic rise in glucose. Plasma noradrenaline rose from 0.29 to 0.59 ng/ml, the rise correlating with the rise in adrenaline. Changes in pulse rate preceded and were unrelated to changes in plasma catecholamines. Fuel mobilisation in response to adrenaline infusion (6 mug/min. for 20 min.) in normoglycaemic man was also studied. Plasma adrenaline concentration rose from a mean of 0.02 ng/ml to 0.71 ng/ml while plasma noradrenaline concentration was unchanged. Blood glucose rose from 71 to 98 mg/100 ml while plasma insulin decreased from 11 to 8 muU/ml. Blood lactate rose by 0.85 mM while pyruvate concentration remained unchanged. Blood glycerol concentration rose twofold and ketone body concentration threefold but there was little change in the concentrations of the glucogenic amino acids, alanine, glutamate and glutamine. Both the 3-hydroxybutyrate/acetoacetate ratio and the lactate/pyruvate ratio rose implying a more reduced intracellular state due presumably to increased hepatic fatty acid oxidation. It is concluded that adrenaline enhances the recycling of lactate and spares glucose through the mobilitsation of lipids but that amino acids are little affected.

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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