Stage fright was used to investigate the mode of action of beta blockers in acute anxiety and on the technical-motor performance of 22 performing string players. They received 100 mg of atenolol or placebo 6.5 hr before performing either in the presence or absence of an audience. Continuous heart rate, stage fright (especially devised rating scale), technical-motor performance (runs of fast notes, trills, vibratos), and urine catecholamine levels were assessed. Before an audience the placebo group showed a significant impairment of technical-motor performance (increase in the relative variance of repeated fast elements of movements: + 25.68%, p less than 0.01) as compared to performance with no audience present; there was a slight but not significant improvement under beta blockade (- 7.48%). Heart rate was significantly lower under beta blockade than under placebo (p less than 0.001). Urine catecholamine levels increased twice as much under beta blockade as under placebo before an audience (p less than 0.01). Beta blockade did not influence stage fright measured before performing, but reduced it (measured immediately after the concert) during the concert. We conclude that the drug was at least partially effective as shown by an improvement in technical-motor performance, and that the beneficial effects of beta blockade in stage fright only involve a peripheral site of action.
47erythroblastopenia of childhood are, indeed, an aged population our findings are inconsistent with a steady exponential decay in the activity of enzymes such as hexokinase and suggest that a rapid loss of enzyme from reticulocytes is followed by relatively little further decline in enzyme activity during the remainder of the red cell life span. Pyrimidine-5'-nucleotidase activity, in contrast, seems to be very largely lost in the first few days of red cell life. with CF. From these observations it was suggested that elevated levels of circulating catecholamines might be responsible for an autonomic dysfunction in CF. Other studies indicated that CF patients have increased cholinergic and a,-adrenergic sensitivity in conjunction with reduced P2-adrenergic responses (12). This assumption was drawn from observations in patients who showed altered pupillary reactivity to physical and chemical stimuli (29), relative insensitivity of blood pressure to beta adrenergic bronchodilatation (9, 18) or altered in vitro results from several CF derived cell preparations (fibroblasts, blood cells, tissue explants) (7,27,32). In contrast, Lake et al. (17) reported normal plasma norepinephrine levels and normal activity of DBH in CF patients. It was speculated, therefore, that neither synthesis nor degradation of catecholamines was affected in CF and, that the observed autonomic dysfunction might not be due to circulating biogenic amines.In view of these conflicting results, the present study was designed to elucidate whether circulating plasma catecholamines, their precursors, metabolites and major urinary products are altered in CF patients and heterozygotes, An attempt was made to correlate these findings to the state of the disease, different blood variables, blood pressure, and heart rate as well as to the sweat electrolyte abnormality. MATERIALS AND METHODS Patients and controls.Blood and 24-h urine samples were collected from 43 children and adolescents with CF (26 boys and 17 girls, range 8-23 yr) attending a summer camp for intensive physiotherapy treatment in a mountain rehabilitation center. All children were treated with the same drug, pancrease (Prolipase), for supplementation of pancreatic insufiiciency, all had the same daily meals and equal daily inhalation therapy with a P2-sympathomimetic drug (hexoprenaline-sulfate, Ipradol). Thirty-five patients received antibiotics orally; no intravenous or further drug therapy was used. All children attended the same physical training and physiotherapy regimen. All children and parents gave informed consent to participate in the study.In 25 parents a single blood specimen could be obtained at the time of admission of the children to the rehabilitation center. Eight healthy adults without a family history of CF served as controls and were investigated at the same time. Values from normal healthy children, collected over several years and measured in the laboratory, performing daily routine catecholamine determinations were randomly selected as age matched and used as contr...
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