Pancreatic trypsin output and plasma secretin and cholecystokinin (CCK) levels were measured in five healthy volunteers to investigate the mechanisms involved in regulating postprandial pancreatic secretion. and CCK by specific radioimmunoassays. Increasing doses of secretin produced increasing bicarbonate output (P < 0.01), whereas trypsin was not stimulated over basal. Graded caerulein produced a stepwise increase in trypsin and bicarbonate output (P < 0.01). Potentiation occurred for bicarbonate secretion between secretin and caerulein, but not for trypsin output. Postprandial trypsin secretion averaged 29.1 IU/min-' over 150 min (equal to 55% of maximal response to caerulein). The peak trypsin response amounted to 90% of maximal caerulein. Significant increases of plasma secretin (P < 0.05) and CCK (P < 0.01) were observed after the meal. Comparison of enzyme and CCK responses to the testmeal or to exogenous caerulein suggested that the amount of CCK released after the meal could account for the postprandial trypsin secretion. We conclude that (a) the postprandial enzyme response in man is submaximal in comparison to maximal exogenous hormone stimulation; (b) CCK is a major stimulatory mechanism of postprandial trypsin secretion, whereas secretin is not involved; and (c) Potentiation of enzyme secretion is not a regulatory mechanism of the postprandial secretory response.

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A considerable proportion of chronic non-organic pain patients suffer from insomnia, and alpha sleep has been suggested to be specifically associated with fibromyalgia. However, the clinical significance of those symptoms is not clear. This study was carried out to investigate this question. Twenty-six middle-aged, non-organic pain patients complaining of persistent insomnia were compared with 25 chronic primary insomniacs in a polysomnographic investigation. Alpha sleep was measured by automatic EEG analysis. A postsleep inventory allowed a separation of those pain patients with actual pain in the recording night to examine its possible influence on sleep. Both groups of patients displayed severe disturbance of sleep maintenance. The pain group did not differ in any of the insomnia variables or in sleep stages from chronic primary insomniacs. The occurrence of alpha sleep was high in either group which suggests that this is not a phenomenon specifically related to pain syndromes. A comparison of the pain subgroups revealed no difference between those with or without actual pain in the recording night. It is concluded that insomnia in chronic pain is of the same type and degree as primary insomnia. Apparently, the chronic process made insomnia so persistent that there was no response to actual night-time pain. Our study suggests that the interpretation of insomnia as secondary to pain, as it is usually made by the pain patients themselves, is a misattribution. It is suggested that insomnia in chronic pain patients should be taken seriously and treated by its specific methods.

Afer an overnight fast a double lumen gastric tube was positioned in the antral part of the stomach under fluoroscopic control. Phenol red (0.1%), a non-absorbable marker, was used to correct for duodenal volume loss11 and instilled into the stomach close to the cardia at a flow rate of 200 ml/h.

No abstract